Entity Extraction Examples (1424)

check_circle_outline   F1 = 100.000
check_circle_outline   F1 >= 50.00
highlight_off   F1 < 50.00
  True Positive  
  False Positive  
  False Negative

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0.9980 CheY - dependent methylation of the asparagine receptor, ProteinMcpB , during chemotaxis in Bacillus subtilis.
0.9196 ProteinCheY - dependent methylation of the asparagine receptor, McpB, during chemotaxis in Bacillus subtilis.
0.7265 CheY - dependent Methylationmethylation of the asparagine receptor, McpB, during chemotaxis in Bacillus subtilis.
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0.9987 For the Gram - positive organism Bacillus subtilis, chemotaxis to the attractant asparagine is mediated by the chemoreceptor ProteinMcpB .
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0.9935 In this study, we show that rapid net demethylation of B. subtilis ProteinMcpB results in the immediate production of methanol, presumably due to the action of CheB.
0.9912 In this study, we show that rapid net demethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of ProteinCheB .
0.6187 In this study, we show that rapid net Methylationdemethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of CheB.
In this study, we show that rapid net Demethylationdemethylation of B. subtilis McpB results in the immediate production of methanol, presumably due to the action of CheB.
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0.9993 We also show that net demethylation of ProteinMcpB occurs upon both addition and removal of asparagine.
0.4519 We also show that net Methylationdemethylation of McpB occurs upon both addition and removal of asparagine.
We also show that net Demethylationdemethylation of McpB occurs upon both addition and removal of asparagine.
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0.9983 After each demethylation event, ProteinMcpB is remethylated to nearly prestimulus levels.
0.8137 After each demethylation event, McpB is Methylationremethylated to nearly prestimulus levels.
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0.9985 Both remethylation events are attributable to ProteinCheR using S - adenosylmethionine as a substrate.
0.8293 Both Methylationremethylation events are attributable to CheR using S - adenosylmethionine as a substrate.
Both Catalysisremethylation events are attributable to CheR using S - adenosylmethionine as a substrate.
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0.9983 Furthermore, we show that the remethylation of asparagine - bound McpB requires the response regulator, CheY - P, suggesting that ProteinCheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis.
0.9972 Furthermore, we show that the remethylation of asparagine - bound McpB requires the response regulator, ProteinCheY - P , suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis.
0.9880 Furthermore, we show that the remethylation of asparagine - bound ProteinMcpB requires the response regulator, CheY - P, suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis.
0.8810 Furthermore, we show that the Methylationremethylation of asparagine - bound McpB requires the response regulator, CheY - P, suggesting that CheY - P acts in a feedback mechanism to facilitate adaptation to positive stimuli during chemotaxis in B. subtilis.
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0.9998 This hypothesis is supported by two observations : a cheRBCD mutant is capable of transient excitation and subsequent oscillations that bring the flagellar rotational bias below the prestimulus value in the tethered cell assay, and the ProteincheRBCD mutant is capable of swarming in a Tryptone swarm plate.
0.9998 This hypothesis is supported by two observations : a ProteincheRBCD mutant is capable of transient excitation and subsequent oscillations that bring the flagellar rotational bias below the prestimulus value in the tethered cell assay, and the cheRBCD mutant is capable of swarming in a Tryptone swarm plate.
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0.9647 Transglycosylation reactions of Bacillus stearothermophilus Proteinmaltogenic amylase with acarbose and various acceptors.
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0.9884 It was observed that Bacillus stearothermophilus Proteinmaltogenic amylase cleaved the first glycosidic bond of acarbose to produce glucose and a pseudotrisaccharide ( PTS ) that was transferred to C - 6 of the glucose to give an alpha - ( 1 - - > 6 ) glycosidic linkage and the formation of isoacarbose.
0.5754 It was observed that Bacillus stearothermophilus maltogenic Proteinamylase cleaved the first glycosidic bond of acarbose to produce glucose and a pseudotrisaccharide ( PTS ) that was transferred to C - 6 of the glucose to give an alpha - ( 1 - - > 6 ) glycosidic linkage and the formation of isoacarbose.
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0.9562 We have purified and characterized a novel high molecular mass glycoprotein of P. chabaudi chabaudi Protein( Pc550gp ) that is transported to the erythrocyte membrane during the intraerythrocytic cycle.
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0.9998 Immuno fluorescence assays with polyclonal monospecific antibodies against ProteinPc550gp show that the protein to be localized in the periphery of young trophozoite stages i. e., on the plasma membrane or parasitophorous vacuole membrane.
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0.9996 Moreover, alkali extraction of purified infected erythrocyte membranes at mature stages of parasite development does not solubilize ProteinPc550gp , suggesting that it is an integral membrane protein.
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0.9996 In addition proteinase K digestion of intact infected host cells induced the disappearance of ProteinPc550gp .
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0.9997 Brefeldin A or low temperature ( 15 degrees C ) treatment did not affect the translocation of ProteinPc550gp from the parasite compartments to the erythrocyte membrane, indicating that the secretion of Pc550gp does not follow the classical transport pathway described in most eukaryotic cells.
0.9996 Brefeldin A or low temperature ( 15 degrees C ) treatment did not affect the translocation of Pc550gp from the parasite compartments to the erythrocyte membrane, indicating that the secretion of ProteinPc550gp does not follow the classical transport pathway described in most eukaryotic cells.
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0.9991 Here, we elucidate two essential steps and describe the roles played by the three translation factors EF - G, RRF, and ProteinIF3 .
0.9982 Here, we elucidate two essential steps and describe the roles played by the three translation factors EF - G, ProteinRRF , and IF3.
0.9976 Here, we elucidate two essential steps and describe the roles played by the three translation factors ProteinEF - G , RRF, and IF3.
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0.9985 Release factor RF3 is known to catalyze the dissociation of RF1 or ProteinRF2 from ribosomes after polypeptide release.
0.9982 Release factor RF3 is known to catalyze the dissociation of ProteinRF1 or RF2 from ribosomes after polypeptide release.
0.9927 Release factor ProteinRF3 is known to catalyze the dissociation of RF1 or RF2 from ribosomes after polypeptide release.
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0.9982 We show that the next step is dissociation of 50S subunits from the 70S posttermination complex and that it is catalyzed by RRF and ProteinEF - G and requires GTP hydrolysis.
0.9965 We show that the next step is dissociation of 50S subunits from the 70S posttermination complex and that it is catalyzed by ProteinRRF and EF - G and requires GTP hydrolysis.
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0.9987 We show that this step requires initiation factor ProteinIF3 , whose role was previously thought to be restricted to promoting specific 30S initiation complex formation from free 30S subunits.
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0.9796 Effect of alternative Glycosylationglycosylation on insulin receptor processing.
0.9509 Effect of alternative glycosylation on Proteininsulin receptor processing.
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0.9803 The mature Proteininsulin receptor is a cell surface heterotetrameric glycoprotein composed of two alpha - and two beta - subunits.
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0.9699 To examine the importance of N - linked glycosylation on Proteininsulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation.
0.9253 To examine the importance of GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation.
0.9429 To examine the importance of N - linked Glycosylationglycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation.
0.7012 To examine the importance of GlycosylationN - linked glycosylation on insulin receptor processing, we have used glucose deprivation as a tool to alter protein glycosylation.
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0.9978 Co - precipitation assays provide evidence that the alternative proreceptor bound ProteinGRP78 , an endoplasmic reticulum molecular chaperone.
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0.9765 N - Glycosidase F treatment shows that the alternative proreceptor contained N - linked Entityoligosaccharides .
0.9545 N - Glycosidase F treatment shows that the alternative proreceptor contained GlycosylationN - linked oligosaccharides.
0.9442 ProteinN - Glycosidase F treatment shows that the alternative proreceptor contained N - linked oligosaccharides.
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0.9492 Yet, Proteinendoglycosidase H insensitivity indicates an aberrant oligosaccharide structure.
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0.9669 Upon refeeding cells that were initially deprived of glucose, the alternative proreceptor was processed to a higher molecular weight form and gained sensitivity to Proteinendoglycosidase H .
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0.9993 Thus far, the focus has been on acetylator genes ( NAT1, ProteinNAT2 ) and the activation of heterocyclic amines, carcinogens generated by cooking meat for prolonged periods at high temperature.
0.9990 Thus far, the focus has been on acetylator genes Protein( NAT1 , NAT2 ) and the activation of heterocyclic amines, carcinogens generated by cooking meat for prolonged periods at high temperature.
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0.9998 Three case - control studies and one prospective study have shown a consistent trend towards higher risks for cancer with higher intakes of meat in rapid acetylators for NAT1, ProteinNAT2 or both genotypes.
0.9998 Three case - control studies and one prospective study have shown a consistent trend towards higher risks for cancer with higher intakes of meat in rapid acetylators for ProteinNAT1 , NAT2 or both genotypes.
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0.9997 Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and ProteinCYP2E1 , respectively, and modulation by meat of the protective effect of the E4 allele of apolipoprotein E on risk for cancer of the proximal colon.
0.9995 Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of ProteinCYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the E4 allele of apolipoprotein E on risk for cancer of the proximal colon.
0.9990 Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the ProteinE4 allele of apolipoprotein E on risk for cancer of the proximal colon.
0.9899 Other links between meat, cooking methods, metabolic genotypes and risk for cancer might include enhanced activation of polycyclic aromatic hydrocarbons and N - nitroso compounds by variant genotypes of CYP1A1 and CYP2E1, respectively, and modulation by meat of the protective effect of the E4 allele of Proteinapolipoprotein E on risk for cancer of the proximal colon.
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0.5464 Differential expression of human Proteinlysyl hydroxylase genes, lysine hydroxylation, and cross - linking of type I collagen during osteoblastic differentiation in vitro.
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0.9991 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 [ PLOD1, ProteinPLOD2 , and PLOD3 ] ).
0.9977 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, Protein2 , and 3 [ PLOD1, PLOD2, and PLOD3 ] ).
0.9963 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and Protein3 [ PLOD1, PLOD2, and PLOD3 ] ).
0.9954 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 [ PLOD1, PLOD2, and ProteinPLOD3 ] ) .
0.9297 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and 3 Protein[ PLOD1 , PLOD2, and PLOD3 ] ).
0.7111 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes Protein( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ).
0.9363 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate, 5 - dioxygenase 1, 2, and Protein3 [ PLOD1 , PLOD2, and PLOD3 ] ).
0.8143 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine, 2 - oxyglutarate Protein, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ).
0.7823 We hypothesized that the tissue specificity of type I collagen cross - linking is, in part, due to the differential expression of lysyl hydroxylase genes ( Procollagen - lysine Protein, 2 - oxyglutarate, 5 - dioxygenase 1 , 2, and 3 [ PLOD1, PLOD2, and PLOD3 ] ).
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0.5110 In addition, using the medium and cell layer / matrix fractions in these cultures, lysine Hydroxylationhydroxylation of type I collagen alpha chains and collagen cross - linking chemistries have been characterized.
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0.9994 High levels of ProteinPLOD1 and PLOD3 genes were expressed in both BMSCs and NSFs, and the expression levels did not change in the course of differentiation.
0.9991 High levels of PLOD1 and ProteinPLOD3 genes were expressed in both BMSCs and NSFs, and the expression levels did not change in the course of differentiation.
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0.9996 In contrast to the ProteinPLOD1 and PLOD3 genes, both cell types showed low PLOD2 gene expression in undifferentiated and early differentiated conditions.
0.9995 In contrast to the PLOD1 and PLOD3 genes, both cell types showed low ProteinPLOD2 gene expression in undifferentiated and early differentiated conditions.
0.9994 In contrast to the PLOD1 and ProteinPLOD3 genes, both cell types showed low PLOD2 gene expression in undifferentiated and early differentiated conditions.
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0.9994 However, fully differentiated BMSCs, but not NSFs, exhibited a significantly elevated level ( 6 - fold increase ) of ProteinPLOD2 mRNA.
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0.9995 The data suggests that ProteinPLOD2 expression is associated with lysine hydroxylation in the nontriple helical domains of collagen and, thus, could be partially responsible for the tissue - specific collagen cross - linking pattern.
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0.9778 Phenylalanine residues in the active site of Proteintyrosine hydroxylase : mutagenesis of Phe300 and Phe309 to alanine and metal ion - catalyzed hydroxylation of Phe300.
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0.9740 Residues Phe300 and Phe309 of Proteintyrosine hydroxylase are located in the active site in the recently described three - dimensional structure of the enzyme, where they have been proposed to play roles in substrate binding.
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0.9693 Mutants of Proteintyrosine hydroxylase with alanine substituted for Phe300 or Phe309 have now been purified and characterized.
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0.9572 The F309A protein possesses 40 % less activity than wild - type Proteintyrosine hydroxylase in the production of DOPA, but full activity in the production of dihydropterin.
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0.8885 The K ( 6 - MPH4 ) value for F300A Proteintyrosine hydroxylase is twice the wild - type value.
0.8410 The K ( 6 - MPH4 ) value for ProteinF300A tyrosine hydroxylase is twice the wild - type value.
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0.7185 Characterization of Phe300 by MALDI - TOF mass spectrometry and amino acid sequencing showed that Hydroxylationhydroxylation only occurs in the isolated catalytic domain after incubation with a large excess of 7, 8 - dihydropterin, DTT, and Fe ( 2 + ).
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0.9967 Development of an enzyme - linked immunosorbent assay, using a monoclonal antibody against Proteinalpha2 - macroglobulin , for the diagnosis of systemic lupus erythematosus.
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0.9908 OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally Glycosylationglycosylated serum alpha2 - macroglobulin ( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ).
0.9501 OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally glycosylated serum alpha2 - macroglobulin Protein( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ).
0.8773 OBJECTIVES : To develop an enzyme - linked immunosorbent assay ( ELISA ) using a monoclonal antibody ( mab ) directed against abnormally glycosylated serum Proteinalpha2 - macroglobulin ( alpha2 - M ) from patients with systemic lupus erythematosus ( SLE ).
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0.9948 DESIGN AND METHODS : Serum alpha2 - M purified by HPLC from patients with SLE was injected in a Balb / c, CB6 F1 female mouse and hybrid cell lines were screened using Proteinalpha2 - M Glu - C fragments derived from SLE and normal donors ( NHS ).
0.9917 DESIGN AND METHODS : Serum Proteinalpha2 - M purified by HPLC from patients with SLE was injected in a Balb / c, CB6 F1 female mouse and hybrid cell lines were screened using alpha2 - M Glu - C fragments derived from SLE and normal donors ( NHS ).
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0.9977 RESULTS : The affinity of the mab for Proteinalpha2 - M from SLE, but not from the other diseases, was higher compared to NHS, as demonstrated by immunoblotting and ELISA.
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0.9920 CONCLUSIONS : The ELISA was capable of recognizing changes of Glycosylationglycosylation of alpha2 - M in SLE and may be useful for its differential diagnosis.
0.9905 CONCLUSIONS : The ELISA was capable of recognizing changes of glycosylation of Proteinalpha2 - M in SLE and may be useful for its differential diagnosis.
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0.9996 These reactions are catalyzed by a dedicated methyltransferase ProteinCheR and a dedicated methylesterase CheB.
0.9987 These reactions are catalyzed by a dedicated methyltransferase CheR and a dedicated methylesterase ProteinCheB .
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0.9996 We investigated the action of ProteinCheB and its activated form, phospho - CheB, on a truncated form of the aspartate receptor of Escherichia coli that was missing the last 5 aa of the intact receptor.
0.9901 We investigated the action of CheB and its activated form, Proteinphospho - CheB , on a truncated form of the aspartate receptor of Escherichia coli that was missing the last 5 aa of the intact receptor.
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0.9997 ProteinCheB bound specifically to an affinity column carrying the isolated pentapeptide, implying that in the intact receptor the pentapeptide serves as a docking site for the methylesterase / deamidase and that the truncated receptor was inefficiently modified because the enzyme could not dock.
0.7522 CheB bound specifically to an affinity column carrying the isolated pentapeptide, implying that in the intact receptor the pentapeptide serves as a docking site for the Proteinmethylesterase / deamidase and that the truncated receptor was inefficiently modified because the enzyme could not dock.
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0.9998 It is striking that the same pentapeptide serves as an activity - enhancing docking site for the methyltransferase ProteinCheR , the other enzyme involved in adaptational covalent modification of chemoreceptors.
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0.9877 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the Proteinp16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.9588 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 Entitypromoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.9485 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island DNA_methylationmethylation and gene transcription.
0.9262 We investigated the kinetics of mRNA induction, demethylation, and DNA_methylationremethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.7222 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between EntityCpG island methylation and gene transcription.
0.7088 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and Entitysecond - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.7960 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon EntityCpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.6599 We investigated the kinetics of mRNA induction, DNA_methylationdemethylation , and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
0.5525 We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between EntityCpG island methylation and gene transcription.
We investigated the kinetics of mRNA induction, DNA_demethylationdemethylation , and remethylation of the p16 promoter and second - exon CpG islands in T24 cells after 5 - aza - 2'- deoxycytidine ( 5 - Aza - CdR ) treatment to explore the relationship between CpG island methylation and gene transcription.
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0.9813 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the Proteinp16 promoter.
0.9664 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and DNA_methylationremethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter.
0.9639 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the Proteinp16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter.
0.9048 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 Entitypromoter .
0.5281 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 Entityexon 2 CpG island occurred at a higher rate than that of the p16 promoter.
0.9509 The rates of DNA_methylationremethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter.
0.6523 The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 EntityCpG island occurred at a higher rate than that of the p16 promoter.
0.5021 The rates of remethylation of both EntityCpG islands were associated with time but not with the rate of cell division, and remethylation of the p16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter.
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0.9825 The kinetics of DNA_methylationremethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9814 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are DNA_methylationhypermethylated in T24 cells.
0.9756 The kinetics of remethylation of the Proteinp16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9712 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and ProteinMYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9666 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, Proteinc - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9610 The kinetics of remethylation of the p16 exon 2, ProteinPAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9118 The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5 , c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.9040 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL Entityexon 11 , and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.8757 The kinetics of remethylation of the p16 Entityexon 2 , PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.8204 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.5206 The kinetics of remethylation of the p16 exon 2, PAX - 6 Entityexon 5, c - ABL exon 11, and MYF - 3 exon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
0.5121 The kinetics of remethylation of the p16 exon 2, PAX - 6 exon 5, c - ABL exon 11, and MYF - 3 Entityexon 3 loci were examined following 5 - Aza - CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells.
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0.9971 Remethylation occurred most rapidly in the p16, PAX - 6, and Proteinc - ABL genes, shown to be transcribed prior to drug treatment.
0.9960 Remethylation occurred most rapidly in the Proteinp16 , PAX - 6, and c - ABL genes, shown to be transcribed prior to drug treatment.
0.9942 Remethylation occurred most rapidly in the p16, ProteinPAX - 6 , and c - ABL genes, shown to be transcribed prior to drug treatment.
0.9563 DNA_methylationRemethylation occurred most rapidly in the p16, PAX - 6, and c - ABL genes, shown to be transcribed prior to drug treatment.
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0.9716 These regions also exhibited higher levels of DNA_methylationremethylation in single - cell clones and subclones derived from 5 - Aza - CdR - treated T24 cells.
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0.9936 Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of ProteinhMLH1 in association of promoter hypermethylation.
0.9859 Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of hMLH1 in association of promoter DNA_methylationhypermethylation .
0.9826 Also, marked relationship of microsatellite instability ( MSI ) and DNA methylation has been reported in sporadic colorectal cancer, which is a result of epigenetic inactivation of hMLH1 in association of Entitypromoter hypermethylation.
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0.9943 In the present study, we investigated the 5'CpG island hypermethylation of hMLH1, E - cadherin and Proteinp16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.9925 In the present study, we investigated the 5'CpG island hypermethylation of hMLH1, ProteinE - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.9907 In the present study, we investigated the 5'CpG island DNA_methylationhypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.9872 In the present study, we investigated the 5'CpG island hypermethylation of ProteinhMLH1 , E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.8857 In the present study, we investigated the Entity5'CpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.8781 In the present study, we investigated the 5 ' EntityCpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.5562 In the present study, we investigated the Entity5'CpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
0.5354 In the present study, we investigated the 5 ' EntityCpG island hypermethylation of hMLH1, E - cadherin and p16 in 61 primary gastric cancers ( GCs ) by using combined bisulfite restriction analysis ( COBRA ) and methylation - specific PCR ( MSP ), and their MSI status.
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0.9895 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed ProteinE - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.9870 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 DNA_methylationmethylation , 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.9851 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented ProteinhMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.9844 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 DNA_methylationmethylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.9795 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and Proteinp16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.8182 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented hMLH1 methylation, 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and DNA_methylationp16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
0.5782 Of 61 GCs investigated, 5 ( 8. 1 % ) tumors presented DNA_methylationhMLH1 methylation , 16 ( 26. 2 % ) and 25 ( 40. 9 % ) showed E - cadherin and p16 methylation respectively, and 8 ( 13. 1 % ) presented high - frequency MSI ( MSI - H ).
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0.9989 Of the 8 MSI - H patients, 5 presented ProteinhMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ).
0.9979 Of the 8 MSI - H patients, 5 presented hMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited ProteinhMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ).
0.9875 Of the 8 MSI - H patients, 5 presented hMLH1 methylation, whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 DNA_methylationmethylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ).
0.9875 Of the 8 MSI - H patients, 5 presented hMLH1 DNA_methylationmethylation , whereas no low - frequency MSI ( MSI - L ) and microsatellite stable ( MSS ) cases exhibited hMLH1 methylation ( 5 / 8 vs. 0 / 43, p < 0. 00001 ).
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0.9964 Furthermore, these patients also presented E - cadherin and Proteinp16 hypermethylation.
0.9959 Furthermore, these patients also presented ProteinE - cadherin and p16 hypermethylation.
0.9495 Furthermore, these patients also presented E - cadherin and p16 DNA_methylationhypermethylation .
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0.9966 Our data showed a significant correlation between ProteinhMLH1 methylation and MSI in GC, and suggested that a common mechanism of aberrant de novo methylation can be postulated in these cancers.
0.9558 Our data showed a significant correlation between hMLH1 DNA_methylationmethylation and MSI in GC, and suggested that a common mechanism of aberrant de novo methylation can be postulated in these cancers.
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0.9781 Effect of ProteinHSP47 on prolyl 4 - hydroxylation of collagen model peptides.
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0.9991 ProteinHSP47 is a collagen - binding stress protein which also resides in the endoplasmic reticulum ( Nagata, K. and Yamada, K. M. ( 1986 ) J.
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0.9912 Both prolyl 4 - hydroxylase and ProteinHSP47 interact with procollagen alpha - chains during their folding and / or modification in the endoplasmic reticulum.
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0.9815 Recent study has revealed that a simple collagen model peptide, ( Pro - Pro - Gly ) n, is recognized by ProteinHSP47 as well as by prolyl 4 - hydroxylase in vitro ( Koide et al., manuscript submitted ).
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0.9723 In the present study, we investigated the effect of ProteinHSP47 on the prolyl 4 - hydroxylation of such collagen model peptides.
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0.9884 When ProteinHSP47 was added to the reaction mixture, substrate and less - hydroxylated materials accumulated.
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0.9971 This effect depended on the peptide - binding activity of HSP47, because a mutant ProteinHSP47 without collagen - binding activity did not show any inhibitory effect on prolyl 4 - hydroxylation.
0.9959 This effect depended on the peptide - binding activity of ProteinHSP47 , because a mutant HSP47 without collagen - binding activity did not show any inhibitory effect on prolyl 4 - hydroxylation.
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0.9830 Kinetic analysis and other biochemical analyses suggest that ProteinHSP47 retards the enzymatic reaction competing for the substrate peptide.
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0.9999 Mouse K - Cl cotransporter ProteinKCC1 : cloning, mapping, pathological expression, and functional regulation.
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0.9989 Although K - Cl cotransporter ( KCC1 ) mRNA is expressed in many tissues, K - Cl cotransport activity has been measured in few cell types, and detection of endogenous ProteinKCC1 polypeptide has not yet been reported.
0.9807 Although K - Cl cotransporter Protein( KCC1 ) mRNA is expressed in many tissues, K - Cl cotransport activity has been measured in few cell types, and detection of endogenous KCC1 polypeptide has not yet been reported.
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0.9998 We have cloned the mouse erythroid KCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the ProteinmKCC1 gene to chromosome 8.
0.9816 We have cloned the mouse erythroid KCC1 Protein( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8.
0.9722 We have cloned the mouse erythroid ProteinKCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8.
0.8525 We have cloned the mouse erythroid ProteinKCC1 ( mKCC1 ) cDNA and its flanking genomic regions and mapped the mKCC1 gene to chromosome 8.
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0.9997 Three anti - peptide antibodies raised against recombinant ProteinmKCC1 function as immunoblot and immunoprecipitation reagents.
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0.9997 The tissue distributions of mKCC1 mRNA and protein are widespread, and ProteinmKCC1 RNA is constitutively expressed during erythroid differentiation of ES cells.
0.9997 The tissue distributions of ProteinmKCC1 mRNA and protein are widespread, and mKCC1 RNA is constitutively expressed during erythroid differentiation of ES cells.
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0.9997 ProteinKCC1 polypeptide or related antigen is present in erythrocytes of multiple species in which K - Cl cotransport activity has been documented.
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0.9978 Erythroid ProteinKCC1 polypeptide abundance is elevated in proportion to reticulocyte counts in density - fractionated cells, in bleeding - induced reticulocytosis, in mouse models of sickle cell disease and thalassemia, and in the corresponding human disorders. mKCC1 - mediated uptake of ( 86 ) Rb into Xenopus oocytes requires extracellular Cl ( - ), is blocked by the diuretic R ( + ) - [ 2 - n - butyl - 6, 7 - dichloro - 2 - cyclopentyl - 2, 3 - dihydro - 1 - oxo - 1H - indenyl - 5 - yl - ) oxy ] acetic acid, and exhibits an erythroid pattern of acute regulation, with activation by hypotonic swelling, N - ethylmaleimide, and staurosporine and inhibition by calyculin and okadaic acid.
0.9933 Erythroid KCC1 polypeptide abundance is elevated in proportion to reticulocyte counts in density - fractionated cells, in bleeding - induced reticulocytosis, in mouse models of sickle cell disease and thalassemia, and in the corresponding human disorders. ProteinmKCC1 - mediated uptake of ( 86 ) Rb into Xenopus oocytes requires extracellular Cl ( - ), is blocked by the diuretic R ( + ) - [ 2 - n - butyl - 6, 7 - dichloro - 2 - cyclopentyl - 2, 3 - dihydro - 1 - oxo - 1H - indenyl - 5 - yl - ) oxy ] acetic acid, and exhibits an erythroid pattern of acute regulation, with activation by hypotonic swelling, N - ethylmaleimide, and staurosporine and inhibition by calyculin and okadaic acid.
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0.9998 These reagents and findings will expedite studies of ProteinKCC1 structure - function relationships and of the pathobiology of KCC1 - mediated K - Cl cotransport.
0.9959 These reagents and findings will expedite studies of KCC1 structure - function relationships and of the pathobiology of ProteinKCC1 - mediated K - Cl cotransport.
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0.8841 Progesterone metabolism in the human kidney and inhibition of Protein11beta - hydroxysteroid dehydrogenase type 2 by progesterone and its metabolites.
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0.8592 Progesterone binds with high affinity to the Proteinmineralocorticoid ( MC ) receptor , but confers only very low agonistic MC activity.
0.6067 Progesterone binds with high affinity to the mineralocorticoid Protein( MC ) receptor , but confers only very low agonistic MC activity.
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One explanation for this phenomenon could be local metabolism of progesterone in the human kidney, similar to the inactivation of cortisol to cortisone by the Protein11beta - hydroxysteroid dehydrogenase ( 11beta - HSD ) type 2 .
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0.8784 Using human kidney cortex microsomes, we tested the inhibitory potency of progesterone and its metabolites on the Protein11beta - HSD type 2 .
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0.9603 In addition to progesterone metabolism by the kidney, the inhibition of Protein11beta - HSD type 2 by progesterone and its metabolites could be a second explanation for the weak MC - antagonist activity of progesterone in vivo.
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0.9710 Inhibition of Protein11beta - HSD type 2 leads to an increase of intracellular cortisol in a way that the local equilibrium between the MC agonist cortisol and the antagonist progesterone is shifted to the agonist side.
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0.9611 INTERVENTION ( S ) : We removed three glycosylation signals from an hCG - hFSH chimera known to have high affinity for LH and ProteinFSH receptors , expecting this would create a bifunctional antagonist ( dgCFC ).
0.9513 INTERVENTION ( S ) : We removed three glycosylation signals from an hCG - hFSH chimera known to have high affinity for ProteinLH and FSH receptors, expecting this would create a bifunctional antagonist ( dgCFC ).
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0.9893 RESULT ( S ) : dgCFC bound LH or ProteinFSH receptors similar to hCG or hFSH.
0.9818 RESULT ( S ) : dgCFC bound ProteinLH or FSH receptors similar to hCG or hFSH.
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0.9476 Regulation of Proteinthyrotropin receptor protein expression in insect cells.
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0.9694 Expression of large quantities of conformationally intact thyrotropin receptor Protein( TSHR ) is essential to understand the structure - function relationship of the receptor.
0.9445 Expression of large quantities of conformationally intact Proteinthyrotropin receptor ( TSHR ) is essential to understand the structure - function relationship of the receptor.
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0.9993 We expressed three different constructs of full - length human ProteinTSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9984 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a ProteinTSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9972 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a ProteinTSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9963 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human ProteinTSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9963 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a ProteinTSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9937 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence Protein( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9901 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence Protein( TSHR - ns ) , ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 ( TSHR - gp ).
0.9901 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence gp - 67 Protein( TSHR - gp ) .
0.7322 We expressed three different constructs of full - length human TSHR in insect cells : ( a ) a TSHR cDNA lacking signal sequence ( TSHR - ns ), ( b ) a TSHR cDNA containing human TSHR signal sequence ( TSHR - hs ) and ( c ) a TSHR cDNA with baculovirus envelope protein encoded signal sequence Proteingp - 67 ( TSHR - gp ).
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0.9996 However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, ProteinTSHR - hs and TSHR - gp virus infected insect cells respectively.
0.9996 However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in ProteinTSHR - ns , TSHR - hs and TSHR - gp virus infected insect cells respectively.
0.9994 However, Western blot using TSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, TSHR - hs and ProteinTSHR - gp virus infected insect cells respectively.
0.9989 However, Western blot using ProteinTSHR specific monoclonal antibody showed unique bands around 80, 100 and 100 kDa in TSHR - ns, TSHR - hs and TSHR - gp virus infected insect cells respectively.
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0.9988 All three full - length ProteinTSHR proteins could neutralize the TSH binding inhibitory immunoglobulin ( TBII ) activity from sera of experimental animals.
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0.9993 However, only glycosylated proteins ( TSHR - hs and ProteinTSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity.
0.9981 However, only glycosylated proteins Protein( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity.
0.9720 However, only Glycosylationglycosylated proteins ( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of glycosylation for patient autoantibody reactivity.
0.8409 However, only glycosylated proteins ( TSHR - hs and TSHR - gp ) neutralized the TBII activity of sera from autoimmune thyroid patients, confirming the importance of Glycosylationglycosylation for patient autoantibody reactivity.
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0.9994 Expression levels of full - length ProteinTSHR proteins were much lower than the levels of similarly produced corresponding ectodomains of TSHR proteins.
0.9990 Expression levels of full - length TSHR proteins were much lower than the levels of similarly produced corresponding ectodomains of ProteinTSHR proteins.
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0.9998 Southern blot and Northern blot analyses showed that DNA and RNA levels in full - length TSHR virus infected insect cells were comparable to the levels found in cells infected with viruses encoding only the ectodomain of ProteinTSHR .
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0.9996 These data suggest that full - length ProteinTSHR expression is very low and is regulated at the translational level.
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0.9996 ProteinBasT , a membrane - bound transducer protein for amino acid detection in Halobacterium salinarum.
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0.9996 We show here that ProteinBasT is a halobacterial transducer protein ( Htp ) responsible for chemotaxis towards five attractant amino acids.
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0.9996 Hydropathy analysis predicts an enterobacterial - type transducer protein topology for ProteinBasT , with an extracellular putative ligand - binding domain flanked by two transmembrane helices and a cytoplasmic domain.
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0.9998 ProteinBasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that BasT is methylatable and membrane bound.
0.9986 BasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that ProteinBasT is methylatable and membrane bound.
0.8197 BasT - inactivated mutant cells are missing a membrane protein radiolabelled with L - [ methyl - 3H ] - methionine in wild - type cells, confirming that BasT is Methylationmethylatable and membrane bound.
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0.9992 Behavioural analysis of the ProteinbasT mutant cells by capillary and chemical - in - plug assays demonstrates complete loss of chemotactic responses towards five ( leucine, isoleucine, valine, methionine and cysteine ) of the six attractant amino acids for Halobacterium salinarum, whereas they still respond to arginine.
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0.9986 The volatile methyl group production assays also corroborate these findings and confirm that ProteinBasT signalling induces methyl group turnover.
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0.9997 Our data identify ProteinBasT as the chemotaxis transducer protein for the branched chain amino acids leucine, isoleucine and valine as well as for methionine and cysteine.
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0.9998 Thus, ProteinBasT and the arginine sensor Car cover the entire spectrum of chemotactic responses towards attractant amino acids in H. salinarum.
0.9991 Thus, BasT and the arginine sensor ProteinCar cover the entire spectrum of chemotactic responses towards attractant amino acids in H. salinarum.
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0.9937 Additional N - glycosylation at Asn ( 13 ) rescues the human ProteinLHbeta - subunit from disulfide - linked aggregation.
0.9927 Additional GlycosylationN - glycosylation at Asn ( 13 ) rescues the human LHbeta - subunit from disulfide - linked aggregation.
0.9679 Additional N - glycosylation at EntityAsn ( 13 ) rescues the human LHbeta - subunit from disulfide - linked aggregation.
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0.9998 Despite the considerable homology between LHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of ProteinLHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta.
0.9998 Despite the considerable homology between ProteinLHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta.
0.9998 Despite the considerable homology between LHbeta and ProteinCGbeta , we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in CGbeta.
0.9997 Despite the considerable homology between LHbeta and CGbeta, we previously demonstrated that, when expressed in GH ( 3 ) cells, the secreted form of LHbeta showed mispaired disulfide - linked aggregation in addition to monomer, whereas no aggregation was observed in ProteinCGbeta .
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0.9996 To determine the domains which are associated with the ProteinLHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition.
0.9994 To determine the domains which are associated with the LHbeta - aggregation and which prevent ProteinCGbeta - aggregation , mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition.
0.9960 To determine the domains which are associated with the LHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in glycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with Proteinanti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition.
0.5586 To determine the domains which are associated with the LHbeta - aggregation and which prevent CGbeta - aggregation, mutant beta - subunits in Glycosylationglycosylation and carboxy - terminus were expressed in GH ( 3 ) cells, and the occurrence of aggregation was assessed by continuous labeling with [ 35S ] methionine / cysteine, immunoprecipitation with anti - hCGbeta serum, and sodium dodecyl sulfate - polyacrylamide gel electrophoresis in a non - reducing condition.
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0.9873 No aggregation was seen when N - linked oligosaccharides were attached to the Asn ( 13 ) of ProteinLHbeta .
0.9754 No aggregation was seen when N - linked oligosaccharides were attached to the EntityAsn ( 13 ) of LHbeta.
0.9257 No aggregation was seen when N - linked Entityoligosaccharides were attached to the Asn ( 13 ) of LHbeta.
0.6661 No aggregation was seen when N - linked oligosaccharides were Glycosylationattached to the Asn ( 13 ) of LHbeta.
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0.9914 Removal of the carbohydrate unit at the EntityAsn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer.
0.9859 Removal of the carbohydrate unit at the Asn ( 13 ) of ProteinCGbeta caused aggregation, although the amount was less than 10 % of monomer.
0.8673 Removal of the Entitycarbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer.
0.4781 DeglycosylationRemoval of the carbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer.
0.8217 Removal of the Entitycarbohydrate unit at the Asn ( 13 ) of CGbeta caused aggregation, although the amount was less than 10 % of monomer.
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0.9987 The carboxy - terminal regions of neither LHbeta nor ProteinCGbeta were associated with their aggregation.
0.9982 The carboxy - terminal regions of neither ProteinLHbeta nor CGbeta were associated with their aggregation.
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0.9988 Both CGbeta wild - type ( WT ) and ProteinCGbeta lacking N - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate.
0.9969 Both ProteinCGbeta wild - type ( WT ) and CGbeta lacking N - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate.
0.9872 Both CGbeta wild - type ( WT ) and CGbeta lacking GlycosylationN - glycosylation at Asn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate.
0.9241 Both CGbeta wild - type ( WT ) and CGbeta lacking N - glycosylation at EntityAsn ( 13 ) ( CGbeta - N13 ) showed aggregates in lysate.
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0.9992 However, in contrast to CGbeta - N13, ProteinCGbetaWT revealed no aggregation in medium.
0.9984 However, in contrast to ProteinCGbeta - N13 , CGbetaWT revealed no aggregation in medium.
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0.9966 These results indicate that the backbone structure consisting of 114 amino acids and N - linked glycosylation at Asn ( 30 ) is involved in the aggregation of ProteinLHbeta .
0.9745 These results indicate that the backbone structure consisting of 114 amino acids and N - linked glycosylation at EntityAsn ( 30 ) is involved in the aggregation of LHbeta.
0.8888 These results indicate that the backbone structure consisting of 114 amino acids and GlycosylationN - linked glycosylation at Asn ( 30 ) is involved in the aggregation of LHbeta.
0.9807 These results indicate that the backbone structure consisting of 114 amino acids and N - linked Glycosylationglycosylation at Asn ( 30 ) is involved in the aggregation of LHbeta.
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0.9965 Moreover, N - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both ProteinLHbeta - and CGbeta - subunits to be secreted as monomer.
0.9960 Moreover, N - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and ProteinCGbeta - subunits to be secreted as monomer.
0.9920 Moreover, GlycosylationN - glycosylation at Asn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and CGbeta - subunits to be secreted as monomer.
0.9863 Moreover, N - glycosylation at EntityAsn ( 13 ) does not prevent such aggregation, but instead plays an important role in correct folding for both LHbeta - and CGbeta - subunits to be secreted as monomer.
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0.9499 ProteinType XIII collagen forms homotrimers with three triple helical collagenous domains and its association into disulfide - bonded trimers is enhanced by prolyl 4 - hydroxylase.
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0.9699 ProteinType XIII collagen is a type II transmembrane protein predicted to consist of a short cytosolic domain, a single transmembrane domain, and three collagenous domains flanked by noncollagenous sequences.
0.6768 Type ProteinXIII collagen is a type II transmembrane protein predicted to consist of a short cytosolic domain, a single transmembrane domain, and three collagenous domains flanked by noncollagenous sequences.
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0.9431 In order to extend studies of Proteintype XIII collagen from cDNAs to the protein level we have produced it in insect cells by means of baculoviruses.
0.5934 In order to extend studies of type ProteinXIII collagen from cDNAs to the protein level we have produced it in insect cells by means of baculoviruses.
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0.9727 Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and Hydroxylationhydroxylation of proline residues dramatically enhanced this association.
0.9044 Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of Entityproline residues dramatically enhanced this association.
0.7708 ProteinType XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of proline residues dramatically enhanced this association.
0.7303 Type XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of Entityproline residues dramatically enhanced this association.
0.6210 ProteinType XIII collagen alpha chains were found to associate into disulfide - bonded trimers, and hydroxylation of proline residues dramatically enhanced this association.
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0.9968 ProteinPepsin and trypsin / chymotrypsin digestions indicated that the type XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation.
0.7930 Pepsin and trypsin / chymotrypsin digestions indicated that the Proteintype XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation.
0.6860 Pepsin and trypsin / chymotrypsin digestions indicated that the Proteintype XIII collagen alpha chains form homotrimers whose three collagenous domains are in triple helical conformation.
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0.9342 All in all, most of the Proteintype XIII collagen ectodomain appears to be present in triple helical conformation, which is in clear contrast to the short or highly interrupted triple helical domains of the other known collagenous transmembrane proteins.
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0.9804 Symmetric and asymmetric DNA methylation in the human ProteinIGF2 - H19 imprinted region.
0.8721 Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region.
0.7417 Symmetric and asymmetric DNA methylation in the human IGF2 - H19 Entityimprinted region .
0.9222 Symmetric and asymmetric DNA DNA_methylationmethylation in the human IGF2 - H19 imprinted region.
0.6758 Symmetric and asymmetric DNA_methylationDNA methylation in the human IGF2 - H19 imprinted region.
0.6149 Symmetric and asymmetric DNA methylation in the human IGF2 - H19 Entityimprinted region.
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0.9989 The two contiguous IGF2 ( human insulin - like growth factor II ) and ProteinH19 genes are reciprocally imprinted in both human and mouse.
0.9986 The two contiguous ProteinIGF2 ( human insulin - like growth factor II ) and H19 genes are reciprocally imprinted in both human and mouse.
0.8282 The two contiguous IGF2 ( human Proteininsulin - like growth factor II ) and H19 genes are reciprocally imprinted in both human and mouse.
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0.9996 In most tissues, IGF2 is transcribed only from the paternal chromosome while ProteinH19 is transcribed only from the maternal allele.
0.9996 In most tissues, ProteinIGF2 is transcribed only from the paternal chromosome while H19 is transcribed only from the maternal allele.
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0.9881 The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5'flanking region of ProteinH19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.9682 The presence of a differential DNA_methylationmethylation region ( DMR ) on the two parental alleles at the 5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.8126 The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.8506 The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5 ' flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.8239 The presence of a differential methylation region ( DMR ) on the two parental alleles at the Entity5'flanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.5867 The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
0.5195 The presence of a differential methylation region ( DMR ) on the two parental alleles at the 5 ' Entityflanking region of H19 has been proposed to constitute the gametic imprint, which controls the reciprocal allelic expression of the two genes.
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0.9914 Using bisulfite genomic sequencing, we have assessed the methylation status of cytosine ( including 154 CpG sites ) in six CpG - rich regions of the human ProteinIGF2 - H19 genes.
0.9168 Using bisulfite genomic sequencing, we have assessed the methylation status of Entitycytosine ( including 154 CpG sites ) in six CpG - rich regions of the human IGF2 - H19 genes.
0.9051 Using bisulfite genomic sequencing, we have assessed the DNA_methylationmethylation status of cytosine ( including 154 CpG sites ) in six CpG - rich regions of the human IGF2 - H19 genes.
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0.9990 In a CpG island near promoter P3 of the ProteinIGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated.
0.9128 In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was DNA_methylationmethylated .
0.6624 In a EntityCpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated.
0.8559 In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all Entitycytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the CpGs was methylated.
0.5444 In a CpG island near promoter P3 of the IGF2 gene, more than 99. 8 % of all cytosines were converted to thymidine by sodium bisulfite mutagenesis, indicating that none of the EntityCpGs was methylated.
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0.9955 In the ProteinIGF2 exon 8 - 9 region, mosaic methylation of 56 CpG sites was observed in fetal tissues and in adult blood DNA.
0.9840 In the IGF2 exon 8 - 9 region, mosaic DNA_methylationmethylation of 56 CpG sites was observed in fetal tissues and in adult blood DNA.
0.6755 In the IGF2 exon 8 - 9 region, mosaic methylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA.
0.5131 In the IGF2 exon 8 - 9 region, mosaic methylation of 56 EntityCpG sites was observed in fetal tissues and in adult blood DNA.
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0.9983 In contrast to the mosaic methylation of ProteinIGF2 , the allelic methylation of the human H19 DMR was uniform.
0.9495 In contrast to the mosaic methylation of IGF2, the allelic DNA_methylationmethylation of the human H19 DMR was uniform.
0.9479 In contrast to the mosaic methylation of IGF2, the allelic methylation of the human ProteinH19 DMR was uniform.
0.9345 In contrast to the mosaic DNA_methylationmethylation of IGF2, the allelic methylation of the human H19 DMR was uniform.
0.8976 In contrast to the mosaic methylation of IGF2, the allelic methylation of the human H19 EntityDMR was uniform.
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0.9967 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the ProteinH19 transcription site, all 25 CpG sites were completely methylated on only one parental allele.
0.9885 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 CpG sites were completely DNA_methylationmethylated on only one parental allele.
0.8887 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele.
0.9163 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely methylated on only one parental allele.
0.5610 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele.
0.5387 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all 25 EntityCpG sites were completely methylated on only one parental allele.
0.5386 In the CpG region located 2 kb upstream ( - 2362 to - 1911 ) of the H19 transcription site, all Entity25 CpG sites were completely methylated on only one parental allele.
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0.9920 Uniform allele - specific DNA_methylationmethylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele.
0.9834 Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete DNA_methylationmethylation of all 25 CpG sites in one parental allele.
0.9734 Uniform allele - specific methylation was also observed in the CpG island proximal to the ProteinH19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele.
0.6477 Uniform allele - specific methylation was also observed in the EntityCpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 CpG sites in one parental allele.
0.7181 Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all 25 EntityCpG sites in one parental allele.
0.5004 Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with DNA_methylationcomplete methylation of all 25 CpG sites in one parental allele.
Uniform allele - specific methylation was also observed in the CpG island proximal to the H19 promoter ( - 711 to - 290 ) with complete methylation of all Entity25 CpG sites in one parental allele.
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0.9850 In contrast, the CpG region in the H19 promoter ( - 292 to + 15 ) was mosaically DNA_methylationmethylated in all tissues.
0.9604 In contrast, the CpG region in the ProteinH19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues.
0.8898 In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues.
0.7647 In contrast, the EntityCpG region in the H19 promoter ( - 292 to + 15 ) was mosaically methylated in all tissues.
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0.9719 In addition, cytosine was DNA_methylationmethylated at three CpNpG and GpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain.
0.9107 In addition, cytosine was methylated at three EntityCpNpG and GpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain.
0.9007 In addition, cytosine was methylated at three CpNpG and EntityGpNpC sites on the top DNA strand and one CpNpG site on the bottom DNA strand from the fetal brain.
0.8889 In addition, cytosine was methylated at three CpNpG and GpNpC sites on the top DNA strand and one EntityCpNpG site on the bottom DNA strand from the fetal brain.
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0.9566 The cytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were DNA_methylationmethylated on only one DNA strand ( asymmetric methylation ).
0.9546 The cytosines at CpG sites were DNA_methylationmethylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ).
0.9444 The cytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while Entitycytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ).
0.9244 The Entitycytosines at CpG sites were methylated on both DNA strands ( symmetric methylation ) while cytosines at the CpNpG and GpNpC sites were methylated on only one DNA strand ( asymmetric methylation ).
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0.9931 The asymmetric methylation was associated with tissue - specific disruption of ProteinH19 genomic imprinting in fetal brain.
0.9505 The asymmetric DNA_methylationmethylation was associated with tissue - specific disruption of H19 genomic imprinting in fetal brain.
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0.9982 An increase in histone acetylation and ProteinIL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production.
0.9969 An increase in histone Acetylationacetylation and IL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production.
0.9952 An increase in Proteinhistone acetylation and IL - 2 antagonizing the immunoinhibitory effect are necessary for augmentation by butyrate of in vitro anti - TNP antibody production.
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0.9977 We investigated the role of Proteinhistone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 ( IL - 2 ).
0.9954 We investigated the role of histone Acetylationacetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 ( IL - 2 ).
0.9559 We investigated the role of histone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus interleukin 2 Protein( IL - 2 ) .
0.8633 We investigated the role of histone acetylation in the promotion of antigen - specific antibody production in murine B cells induced by sodium butyrate ( NaBu ) plus Proteininterleukin 2 ( IL - 2 ).
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0.9978 NaBu dose dependently increased the acetylation levels of histone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of ProteinIL - 2 .
0.9956 NaBu dose dependently increased the Acetylationacetylation levels of histone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of IL - 2.
0.9652 NaBu dose dependently increased the acetylation levels of Proteinhistone H4 at concentrations which effectively enhanced anti - trinitrophenyl ( TNP ) antibody production in the presence of IL - 2.
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0.9955 Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of ProteinIL - 2 in increasing both antibody production and the histone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2.
0.9955 Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the histone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of ProteinIL - 2 .
0.9899 Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the histone H4 Acetylationacetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2.
0.9753 Among other short - chain fatty acids and NaBu analogs, propionate, valerate and vinylacetate were effective in the presence of IL - 2 in increasing both antibody production and the Proteinhistone H4 acetylation level, but acetate, alpha -, beta - and gamma - hydroxybutyrates and alpha -, beta - and gamma - aminobutyrates were not effective, even in the presence of IL - 2.
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0.9988 The effect of the specific histone deacetylase inhibitor trichostatin A ( TSA ), which enhances anti - TNP antibody production without ProteinIL - 2 , was markedly inhibited by adding NaBu simultaneously.
0.9979 The effect of the specific Proteinhistone deacetylase inhibitor trichostatin A ( TSA ), which enhances anti - TNP antibody production without IL - 2, was markedly inhibited by adding NaBu simultaneously.
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0.9977 However, the effect of TSA was neither inhibited nor potentiated by NaBu in the presence of ProteinIL - 2 .
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0.9962 Splenic B cells treated with NaBu, TSA and both together in the presence or absence of IL - 2 showed almost the same increased Acetylationacetylation level of histone H4.
0.9855 Splenic B cells treated with NaBu, TSA and both together in the presence or absence of ProteinIL - 2 showed almost the same increased acetylation level of histone H4.
0.9659 Splenic B cells treated with NaBu, TSA and both together in the presence or absence of IL - 2 showed almost the same increased acetylation level of Proteinhistone H4 .
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0.9997 These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of histone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by ProteinIL - 2 .
0.9987 These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of ProteinIL - 2 is mediated through a moderate increase in the level of histone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2.
0.9973 These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of histone Acetylationacetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2.
0.9956 These results suggest that the NaBu - induced enhancement of anti - TNP antibody production in the presence of IL - 2 is mediated through a moderate increase in the level of Proteinhistone acetylation and that NaBu has both stimulating and inhibiting activities for anti - TNP antibody production, the latter of which is overcome by IL - 2.
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0.9952 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ProteinORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ).
0.9944 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA Protein( ORF73 - IFA and K8. 1 - IFA ).
0.9680 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and ProteinK8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ).
0.8660 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and ProteinK8. 1 - IFA ) .
0.8664 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8 Protein. 1 - IFA ) .
0.8454 To provide more reliable IFAs, we established recombinant Semliki Forest viruses ( rSFVs ) expressing the HHV - 8 - specific proteins ORF73 and K8 Protein. 1 and used BHK - 21 cells infected with these rSFVs for IFA ( ORF73 - IFA and K8. 1 - IFA ).
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0.8599 The rSFV system also allowed detection of antibodies against glycosylation - dependent epitopes of ProteinK8. 1 .
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0.9991 K8. 1 - IFA was more sensitive than either ProteinORF73 - IFA or peptide ELISAs.
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0.9467 Using PEL - based lytic IFA as a reference assay, the sensitivity and specificity of ProteinK8. 1 - IFA were estimated to be 94 and 100 %, respectively.
0.8804 Using PEL - based lytic IFA as a reference assay, the sensitivity and specificity of K8 Protein. 1 - IFA were estimated to be 94 and 100 %, respectively.
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0.9696 HHV - 8 prevalences determined by ProteinK8. 1 - IFA among the human immunodeficiency virus ( HIV ) - positive ( HIV ( + ) ) Kaposi's sarcoma ( KS ) patients, HIV ( + ) KS ( - ) patients, and healthy controls were 100, 65, and 6. 7 %, respectively, which were consistent with prior reports.
0.9475 HHV - 8 prevalences determined by K8 Protein. 1 - IFA among the human immunodeficiency virus ( HIV ) - positive ( HIV ( + ) ) Kaposi's sarcoma ( KS ) patients, HIV ( + ) KS ( - ) patients, and healthy controls were 100, 65, and 6. 7 %, respectively, which were consistent with prior reports.
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0.9937 Evidence that the lizard Proteinhelospectin peptides are O - glycosylated.
0.9909 Evidence that the lizard helospectin peptides are GlycosylationO - glycosylated .
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0.9973 Six forms of Proteinhelospectin ( a vasoactive intestinal peptide analogue ) were purified from the venom of the Heloderma horridum lizard.
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0.9993 Two forms were identified as the previously named ProteinHs1 and Hs2 of 38 and 37 amino - acid residues, respectively.
0.9988 Two forms were identified as the previously named Hs1 and ProteinHs2 of 38 and 37 amino - acid residues, respectively.
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0.9626 Two forms corresponded to Hs1 and Hs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the EntitySer32 residue.
0.9589 Two forms corresponded to ProteinHs1 and Hs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue.
0.9497 Two forms corresponded to Hs1 and Hs2 O - glycosylated by a EntityN - acetylhexosamine - hexose motif attached to the Ser32 residue.
0.9493 Two forms corresponded to Hs1 and Hs2 GlycosylationO - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue.
0.9234 Two forms corresponded to Hs1 and ProteinHs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue.
0.6560 Two forms corresponded to Hs1 and GlycosylationHs2 O - glycosylated by a N - acetylhexosamine - hexose motif attached to the Ser32 residue.
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0.8040 Two other forms were not completely characterized but might correspond to the GlycosylationO - glycosylated forms bearing a phosphate or a sulfate group.
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0.9992 The glycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat ProteinVPAC1 and VPAC2 receptors.
0.9992 The glycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat VPAC1 and ProteinVPAC2 receptors.
0.9919 The glycosylation did not affect the capacity of the Proteinhelospectins to recognize and to activate the human and the rat VPAC1 and VPAC2 receptors.
0.9814 The Glycosylationglycosylation did not affect the capacity of the helospectins to recognize and to activate the human and the rat VPAC1 and VPAC2 receptors.
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0.9985 Liver - specific and non - liver - specific methionine adenosyltransferase ( MAT ) are products of two genes, MAT1A and ProteinMAT2A , respectively, that catalyze the formation of S - adenosylmethionine ( SAM ).
0.9983 Liver - specific and non - liver - specific methionine adenosyltransferase ( MAT ) are products of two genes, ProteinMAT1A and MAT2A, respectively, that catalyze the formation of S - adenosylmethionine ( SAM ).
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0.9971 We previously showed that ProteinMAT2A expression was associated with more rapid cell growth.
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0.9981 After rats were fed intragastrically with ethanol and high fat for 9 wk, the mRNA level of both MAT forms doubled but only the protein level of ProteinMAT2A increased.
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0.9997 Hepatic levels of methionine, SAM, and DNA methylation fell by approximately 40 %. Proteinc - myc was hypomethylated, and its mRNA level increased.
0.9195 Hepatic levels of methionine, SAM, and DNA methylation fell by approximately 40 %. c - myc was DNA_methylationhypomethylated , and its mRNA level increased.
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0.9998 Thus in the prefibrotic stage of alcoholic liver injury, there is already a switch in MAT expression, global DNA hypomethylation, increased Proteinc - myc expression, and genome - wide DNA strand break.
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0.9994 Hsl7p, the yeast homologue of human ProteinJBP1 , is a protein methyltransferase.
0.9994 ProteinHsl7p , the yeast homologue of human JBP1, is a protein methyltransferase.
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0.9996 The yeast protein ProteinHsl7p is a homologue of Janus kinase binding protein 1, JBP1, a newly characterized protein methyltransferase.
0.9993 The yeast protein Hsl7p is a homologue of Janus kinase binding protein 1, ProteinJBP1 , a newly characterized protein methyltransferase.
0.7987 The yeast protein Hsl7p is a homologue of ProteinJanus kinase binding protein 1 , JBP1, a newly characterized protein methyltransferase.
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0.9996 In this report, ProteinHsl7p also is shown to be a methyltransferase.
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0.9970 Calf histones H2A and H4 and bovine myelin basic protein were methylated by ProteinHsl7p , whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
0.9893 Calf histones H2A and ProteinH4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
0.9845 Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, ProteinH2B , and H3 and bovine cytochrome c were not.
0.9780 Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and ProteinH3 and bovine cytochrome c were not.
0.9716 Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas Proteinhistones H1 , H2B, and H3 and bovine cytochrome c were not.
0.9619 Calf Proteinhistones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
0.9281 Calf histones H2A and H4 and bovine myelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine Proteincytochrome c were not.
0.9184 Calf histones H2A and H4 and bovine Proteinmyelin basic protein were methylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
0.6789 Calf histones H2A and H4 and bovine myelin basic protein were Catalysismethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
Calf histones H2A and H4 and bovine myelin basic protein were Methylationmethylated by Hsl7p, whereas histones H1, H2B, and H3 and bovine cytochrome c were not.
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0.9999 We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by ProteinJBP1 .
0.9999 We demonstrated that ProteinJBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1.
0.9997 We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted ProteinHSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the JBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1.
0.9994 We demonstrated that JBP1 can complement Saccharomyces cerevisiae with a disrupted HSL7 gene as judged by a reduction of the elongated bud phenotype, and a point mutation in the ProteinJBP1 S - adenosylmethionine consensus binding sequence eliminated all complementation by JBP1.
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0.9998 Therefore, we conclude the yeast protein Hsl7p is a sequence and functional homologue of ProteinJBP1 .
0.9998 Therefore, we conclude the yeast protein ProteinHsl7p is a sequence and functional homologue of JBP1.
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0.9962 Rapid induction of Proteinhistone hyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase - 1.
0.9450 Rapid induction of histone Acetylationhyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase - 1.
0.6429 Rapid induction of histone hyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of Proteinhistone deacetylase - 1 .
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0.9385 The cells accumulated lipid droplets, and the Proteincytokeratin 18 cytoskeleton was reorganized.
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0.9712 AcetylationHyperacetylated histone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h.
0.9591 Hyperacetylated Proteinhistone H4 appeared within 2 h of the addition of quinidine to the medium, and levels were maximal by 24 h.
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0.9877 Quinidine - treated MCF - 7 cells showed elevated Proteinp21 ( WAF1 ) , hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.
0.9867 Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by Proteinhistone deacetylase inhibitors, trichostatin A, and trapoxin.
0.9713 Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of Proteinretinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.
0.9423 Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), hypophosphorylation and suppression of retinoblastoma protein, and down - regulation of Proteincyclin D1 , similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.
0.9187 Quinidine - treated MCF - 7 cells showed elevated p21 ( WAF1 ), Phosphorylationhypophosphorylation and suppression of retinoblastoma protein, and down - regulation of cyclin D1, similar to the cell cycle response observed with cells induced to differentiate by histone deacetylase inhibitors, trichostatin A, and trapoxin.
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0.9988 Quinidine did not show evidence for direct inhibition of Proteinhistone deacetylase enzymatic activity in vitro.
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0.9994 ProteinHDAC1 was undetectable in MCF - 7 cells 30 min after addition of quinidine to the growth medium.
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0.9994 The proteasome inhibitors MG - 132 and lactacystin completely protected ProteinHDAC1 from the action of quinidine.
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0.9998 We conclude that quinidine is a breast tumor cell differentiating agent that causes the loss of ProteinHDAC1 via a proteasomal sensitive mechanism.
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0.9996 The ProteinKvLQT1 and minK subunits that coassemble to form I ( sK ) channels, contain potential N - glycosylation sites.
0.9992 The KvLQT1 and ProteinminK subunits that coassemble to form I ( sK ) channels, contain potential N - glycosylation sites.
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0.9930 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat Protein( rminK ) or human minK ( hminK ) cDNA.
0.9878 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human ProteinKvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA.
0.9802 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human ProteinminK ( hminK ) cDNA.
0.9755 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK Protein( hminK ) cDNA.
0.9669 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 Protein( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA.
0.9427 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human ProteinminK ( hminK ) cDNA.
0.9248 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in glycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human ProteinKvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA.
0.6275 To examine the role of glycosylation in channel function, a Chinese hamster ovary cell line deficient in Glycosylationglycosylation ( Lec - 1 ) and its parental cell line ( Pro - 5 ) were transiently transfected with human KvLQT1 ( hKvLQT1 ) cDNA, alone and in combination with the rat ( rminK ) or human minK ( hminK ) cDNA.
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0.9996 Functional KvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with ProteinhKvLQT1 and hKvLQT1 / hminK.
0.9995 Functional KvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with hKvLQT1 and ProteinhKvLQT1 / hminK .
0.9994 Functional ProteinKvLQT1 and I ( sK ) currents were expressed in both cell lines, although amplitudes were larger in Pro - 5 than Lec - 1 cells transfected with hKvLQT1 and hKvLQT1 / hminK.
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0.9997 For I ( sK ), but not ProteinKvLQT1 , the voltage - dependence of activation was shifted to more positive voltages and the activation kinetics were slower in the Lec - 1 compared to the Pro - 5 cells.
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0.9997 The effect of extracellular acidification on recombinant ProteinKvLQT1 and I ( sK ) currents was investigated in Pro - 5 and Lec - 1 cells.
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0.9998 Changing external pH ( pH ( o ) ) from 7. 4 to 6. 0 significantly decreased the amplitude and increased the half - activation voltage ( V ( 1 / 2 ) ) of ProteinKvLQT1 currents in Pro - 5 and Lec - 1 cells.
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0.9998 In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether rminK or ProteinhminK was coexpressed with hKvLQT.
0.9997 In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether ProteinrminK or hminK was coexpressed with hKvLQT.
0.9997 In Pro - 5 cells, decreasing pH ( o ) reduced I ( sK ) amplitude without increasing V ( 1 / 2 ), whether rminK or hminK was coexpressed with ProteinhKvLQT .
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0.9940 Thus, oligosaccharides attached to the ProteinminK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ).
0.9781 Thus, Entityoligosaccharides attached to the minK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ).
0.8683 Thus, oligosaccharides Glycosylationattached to the minK subunit affect not only the gating properties, but also the pH sensitivity of I ( sK ).
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0.9461 A novel post - translational modification of yeast Proteinelongation factor 1A . Methylesterification at the C terminus.
0.6711 A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C Entityterminus.
0.7514 A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C Entityterminus .
0.6105 A novel post - translational modification of yeast elongation factor 1A. Methylesterification at the C terminus Entity.
0.5136 A novel post - translational modification of yeast elongation factor 1A. MethylationMethylesterification at the C terminus.
A novel post - translational modification of yeast elongation factor 1A. Methylesterification Methylationat the C terminus.
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0.9972 Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic elongation factor 1A ( eEF1A, formerly ProteinEF - 1alpha ) , the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation.
0.9606 Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic elongation factor 1A Protein( eEF1A , formerly EF - 1alpha ), the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation.
0.8489 Peptide sequence analysis of the purified methylated protein revealed that it is eukaryotic Proteinelongation factor 1A ( eEF1A, formerly EF - 1alpha ), the protein that forms a complex with GTP and aminoacyl - tRNAs for binding to the ribosomal A site during protein translation.
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0.9971 Previous studies have shown that ProteineEF1A is methylated on several internal lysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives.
0.9474 Previous studies have shown that eEF1A is Methylationmethylated on several internal lysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives.
0.9245 Previous studies have shown that eEF1A is methylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives.
0.6905 Previous studies have shown that eEF1A is methylated on several internal Entitylysine residues to give mono -, di -, and tri - N - epsilon - methyl - lysine derivatives.
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0.5146 We confirm this finding but also detect Methylationmethylation that is released as volatile methyl groups after base hydrolysis, characteristic of ester linkages.
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0.9973 In cycloheximide - treated cells, methyl esterified ProteineEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction.
0.9578 In cycloheximide - treated cells, methyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no Methylationmethylated protein was found in the soluble fraction.
0.8917 In cycloheximide - treated cells, Methylationmethyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction.
0.9208 In cycloheximide - treated cells, Methylationmethyl esterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction.
0.9066 In cycloheximide - treated cells, methyl Methylationesterified eEF1A was detected largely in the ribosome and polysome fractions ; little or no methylated protein was found in the soluble fraction.
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0.9985 Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of ProteineEF1A could be released by trypsin treatment but not by carboxypeptidase Y or chymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue.
0.9895 Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of eEF1A could be released by trypsin treatment but not by carboxypeptidase Y or Proteinchymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue.
0.9726 Because the base - labile, volatile [ methyl - ( 3 ) H ] radioactivity of eEF1A could be released by trypsin treatment but not by Proteincarboxypeptidase Y or chymotrypsin treatment, we suggest that the methyl ester is present on the alpha - carboxyl group of its C - terminal lysine residue.
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0.9822 From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated lysine residues of ProteineEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min.
0.9752 From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated lysine residues of eEF1A are stable over 4 h, whereas the ProteineEF1A carboxyl methyl ester has a half - life of less than 10 min.
0.9606 From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min.
0.9305 From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the MethylationN - methylated lysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min.
0.9633 From the results of pulse - chase experiments using radiolabeled intact yeast cells, we find that the N - methylated Entitylysine residues of eEF1A are stable over 4 h, whereas the eEF1A carboxyl methyl ester has a half - life of less than 10 min.
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0.9869 The rapid turnover of the methyl ester suggests that the methylation / demethylation of ProteineEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
0.8168 The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
0.6890 The rapid turnover of the methyl ester suggests that the Methylationmethylation / demethylation of eEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
0.6115 The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
0.5162 The rapid turnover of the methyl ester suggests that the methylation / demethylation of eEF1A at the EntityC - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
The rapid turnover of the methyl ester suggests that the Demethylationmethylation / demethylation of eEF1A at the C - terminal carboxyl group may represent a novel mode of regulation of the activity of this protein in yeast.
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0.9997 Decreased UDP - GlcNAc levels abrogate proliferation control in ProteinEMeg32 - deficient cells.
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0.9974 We have recently identified the murine glucosamine - 6 - phosphate ( GlcN6P ) acetyltransferase, ProteinEMeg32 , as a developmentally regulated enzyme on the route to UDP - N : - acetylglucosamine ( UDP - GlcNAc ).
We have recently identified the murine Proteinglucosamine - 6 - phosphate ( GlcN6P ) acetyltransferase , EMeg32, as a developmentally regulated enzyme on the route to UDP - N : - acetylglucosamine ( UDP - GlcNAc ).
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0.9995 Here we describe embryos and cells that have the ProteinEMeg32 gene inactivated by homologous recombination.
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0.9943 In vitro differentiated ProteinEMeg32 ( - / - ) ES cells show reduced proliferation.
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0.9998 Mouse embryonic fibroblasts ( MEFs ) deficient for EMeg32 exhibit defects in proliferation and adhesiveness, which could be complemented by stable re - expression of ProteinEMeg32 or by nutritional restoration of intracellular UDP - GlcNAc levels.
0.9997 Mouse embryonic fibroblasts ( MEFs ) deficient for ProteinEMeg32 exhibit defects in proliferation and adhesiveness, which could be complemented by stable re - expression of EMeg32 or by nutritional restoration of intracellular UDP - GlcNAc levels.
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0.9994 Interestingly, growth - impaired EMeg32 ( - / - ) MEFs withstand a number of apoptotic stimuli and express activated ProteinPKB / AKT .
0.9876 Interestingly, growth - impaired ProteinEMeg32 ( - / - ) MEFs withstand a number of apoptotic stimuli and express activated PKB / AKT.
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0.9572 Thus, ProteinEMeg32 - dependent UDP - GlcNAc levels influence cell cycle progression and susceptibility to apoptotic stimuli.
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0.9851 Post - translational hydroxylation at the EntityN - terminus of the prion protein reveals presence of PPII structure in vivo.
0.9833 Post - translational Hydroxylationhydroxylation at the N - terminus of the prion protein reveals presence of PPII structure in vivo.
0.8842 Post - translational hydroxylation at the N - terminus of the Proteinprion protein reveals presence of PPII structure in vivo.
0.5360 Post - translational hydroxylation at the N - terminus of the Proteinprion protein reveals presence of PPII structure in vivo.
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0.9991 The transmissible spongiform encephalopathies are characterized by conversion of a host protein, ProteinPrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, PrP ( Sc ) ( prion protein scrapie isoform ).
0.9858 The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, ProteinPrP ( Sc ) ( prion protein scrapie isoform ).
0.9844 The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular Proteinprion protein ) , to a protease - resistant isoform, PrP ( Sc ) ( prion protein scrapie isoform ).
0.8187 The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, ProteinPrP ( Sc ) ( prion protein scrapie isoform ).
The transmissible spongiform encephalopathies are characterized by conversion of a host protein, PrP ( C ) ( cellular prion protein ), to a protease - resistant isoform, PrP ( Sc ) Protein( prion protein scrapie isoform ).
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0.9991 The importance of the highly flexible, N - terminal region of ProteinPrP has recently become more widely appreciated, particularly the biological activities associated with its metal ion - binding domain and its potential to form a poly ( L - proline ) II ( PPII ) helix.
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0.9977 Circular dichroism spectroscopy of an N - terminal peptide, ProteinPrP ( 37 - 53 ) , showed that the PPII helix is formed in aqueous buffer ; as it also contains an Xaa - Pro - Gly consensus sequence, it may act as a substrate for the collagen - modifying enzyme prolyl 4 - hydroxylase.
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0.9999 Direct evidence for this modification was obtained by mass spectrometry and Edman sequencing in recombinant mouse ProteinPrP secreted from stably transfected Chinese hamster ovary cells.
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0.9822 Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in ProteinPrP ( Sc ) from the brains of scrapie - infected mice.
0.9815 Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same Hydroxylationhydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice.
0.9782 Almost complete conversion of proline to 4 - hydroxyproline occurs specifically at residue EntityPro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice.
0.8374 Almost complete Hydroxylationconversion of proline to 4 - hydroxyproline occurs specifically at residue Pro44 of this murine protein ; the same hydroxylated residue was detected, at lower levels, in PrP ( Sc ) from the brains of scrapie - infected mice.
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0.9961 Cation binding and / or post - translational hydroxylation of this region of ProteinPrP may regulate its role in the physiology and pathobiology of the cell.
0.9453 Cation binding and / or post - translational Hydroxylationhydroxylation of this region of PrP may regulate its role in the physiology and pathobiology of the cell.
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0.9998 Carboxymethylation of the PP2A catalytic subunit in Saccharomyces cerevisiae is required for efficient interaction with the B - type subunits Cdc55p and ProteinRts1p .
0.9998 Carboxymethylation of the PP2A catalytic subunit in Saccharomyces cerevisiae is required for efficient interaction with the B - type subunits ProteinCdc55p and Rts1p.
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0.9987 We have used the budding yeast Saccharomyces cerevisiae as a model system to investigate the hypothesis that covalent modification of the C subunit Protein( Pph21p / Pph22p ) carboxyl terminus modulates PP2A complex formation.
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0.9999 First, S. cerevisiae cells were generated whose survival depended on the expression of different carboxyl - terminal ProteinPph21p mutants.
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0.9643 Second, the major S. cerevisiae methyltransferase Protein( Ppm1p ) that catalyzes the methylation of the PP2A C subunit carboxyl - terminal leucine was identified, and cells deleted for this methyltransferase were utilized for our studies.
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0.9997 Our results demonstrate that binding of the yeast B subunit, Cdc55p, to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on ProteinPph21p or by deletion of the gene for Ppm1p.
0.9996 Our results demonstrate that binding of the yeast B subunit, Cdc55p, to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for ProteinPpm1p .
0.9996 Our results demonstrate that binding of the yeast B subunit, ProteinCdc55p , to Pph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for Ppm1p.
0.9996 Our results demonstrate that binding of the yeast B subunit, Cdc55p, to ProteinPph21p was disrupted by either acidic substitution of potential carboxyl - terminal phosphorylation sites on Pph21p or by deletion of the gene for Ppm1p.
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0.9998 Loss of Cdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, ProteinTpd3p , to Pph21p.
0.9995 Loss of ProteinCdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, Tpd3p, to Pph21p.
0.9995 Loss of Cdc55p association was accompanied in each case by a large reduction in binding of the yeast A subunit, Tpd3p, to ProteinPph21p .
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0.9998 Moreover, decreased Cdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or ProteinTPD3 deletion.
0.9998 Moreover, decreased ProteinCdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or TPD3 deletion.
0.9997 Moreover, decreased Cdc55p and Tpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of ProteinCDC55 or TPD3 deletion.
0.9997 Moreover, decreased Cdc55p and ProteinTpd3p binding invariably resulted in nocodazole sensitivity, a known phenotype of CDC55 or TPD3 deletion.
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0.9992 Furthermore, loss of methylation also greatly reduced the association of another yeast B - type subunit, ProteinRts1p .
0.4138 Furthermore, loss of DNA_methylationmethylation also greatly reduced the association of another yeast B - type subunit, Rts1p.
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0.9986 Thus, methylation of ProteinPph21p is important for formation of PP2A trimeric and dimeric complexes, and consequently, for PP2A function.
0.7999 Thus, Methylationmethylation of Pph21p is important for formation of PP2A trimeric and dimeric complexes, and consequently, for PP2A function.
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0.9982 OUTCOME MEASURES : Safety parameters, evaluated at each dose level, included measurement of total testosterone, free testosterone, dihydrotestosterone, estradiol, cortisol, thyroxin and Proteininsulin levels.
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0.9362 ProteinAureusidin synthase : a polyphenol oxidase homolog responsible for flower coloration.
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0.9690 The enzyme Protein( aureusidin synthase ) is a 39 - kilodalton, copper - containing glycoprotein catalyzing the hydroxylation and / or oxidative cyclization of the precursor chalcones, 2 ', 4 ', 6 ', 4 - tetrahydroxychalcone and 2 ', 4 ', 6 ', 3, 4 - pentahydroxychalcone.
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0.9674 The complementary DNA encoding Proteinaureusidin synthase is expressed in the petals of aurone - containing varieties.
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0.9838 DNA sequence analysis revealed that Proteinaureusidin synthase belongs to the plant polyphenol oxidase family, providing an unequivocal example of the function of the polyphenol oxidase homolog in plants, i. e., flower coloration.
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0.9934 ProteinE - cadherin expression is silenced by 5'CpG island methylation in acute leukemia.
0.9906 E - cadherin expression is silenced by 5'CpG island DNA_methylationmethylation in acute leukemia.
0.5636 E - cadherin expression is silenced by Entity5'CpG island methylation in acute leukemia.
0.5725 E - cadherin expression is silenced by 5 ' EntityCpG island methylation in acute leukemia.
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0.9964 ProteinE - Cadherin is a transmembrane glycoprotein that mediates Ca2 + - dependent intercellular adhesion in normal epithelium.
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0.9996 In tumors of epithelial origin, ProteinE - cadherin expression frequently is reduced, an event that contributes to tumor invasion and metastasis.
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0.9996 The role of ProteinE - cadherin in hematopoietic tissues is less clear.
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0.9996 In normal bone marrow, ProteinE - cadherin is expressed on erythroid progenitors, CD34 + stem cells, and stromal cells, where it likely contributes to intercellular interactions during hematopoiesis.
0.9993 In normal bone marrow, E - cadherin is expressed on erythroid progenitors, ProteinCD34 + stem cells, and stromal cells, where it likely contributes to intercellular interactions during hematopoiesis.
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0.9914 In this study, we used a nested - PCR approach to examine the DNA_methylationmethylation status of the E - cadherin 5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
0.9515 In this study, we used a nested - PCR approach to examine the methylation status of the ProteinE - cadherin 5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
0.7872 In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
0.8178 In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
0.7121 In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin 5 ' EntityCpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
0.5629 In this study, we used a nested - PCR approach to examine the methylation status of the E - cadherin Entity5'CpG island in blood and bone marrow samples from normal donors and in bone marrow from patients with acute leukemia.
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0.9986 In normal peripheral blood mononuclear cells and bone marrow, ProteinE - cadherin was completely unmethylated.
0.9065 In normal peripheral blood mononuclear cells and bone marrow, E - cadherin was completely DNA_methylationunmethylated .
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0.9995 Immunoblotting confirmed ProteinE - cadherin protein expression in two lymphoblastoid cell lines derived from normal donors.
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0.9978 In contrast, ProteinE - cadherin was aberrantly methylated in 4 of 4 ( 100 % ) leukemia cell lines, 14 of 44 ( 32 % ) acute myelogenous leukemias, and 18 of 33 ( 53 % ) acute lymphoblastic leukemias.
0.9778 In contrast, E - cadherin was aberrantly DNA_methylationmethylated in 4 of 4 ( 100 % ) leukemia cell lines, 14 of 44 ( 32 % ) acute myelogenous leukemias, and 18 of 33 ( 53 % ) acute lymphoblastic leukemias.
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0.9793 Genomic bisulfite sequencing of primary leukemias confirmed dense DNA_methylationmethylation across the CpG island.
0.7436 Genomic bisulfite sequencing of primary leukemias confirmed dense methylation across the EntityCpG island .
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0.9986 Methylation was associated with loss of ProteinE - cadherin RNA and protein in leukemia cell lines and primary leukemias.
0.9860 DNA_methylationMethylation was associated with loss of E - cadherin RNA and protein in leukemia cell lines and primary leukemias.
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0.9989 Following treatment with 5 - aza - 2'- deoxycytidine, a methylated leukemia cell line expressed both ProteinE - cadherin transcript and protein.
0.9633 Following treatment with 5 - aza - 2'- deoxycytidine, a DNA_methylationmethylated leukemia cell line expressed both E - cadherin transcript and protein.
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0.9992 Our results show that methylation of ProteinE - cadherin occurs commonly in acute leukemia and suggests a hypothesis for E - cadherin down - regulation in leukemogenesis.
0.9991 Our results show that methylation of E - cadherin occurs commonly in acute leukemia and suggests a hypothesis for ProteinE - cadherin down - regulation in leukemogenesis.
0.9513 Our results show that DNA_methylationmethylation of E - cadherin occurs commonly in acute leukemia and suggests a hypothesis for E - cadherin down - regulation in leukemogenesis.
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0.9882 Hypoglycosylated forms of Proteinalpha1 - antitrypsin have been detected by Western blot in serum from CDG Ia patients.
0.7849 GlycosylationHypoglycosylated forms of alpha1 - antitrypsin have been detected by Western blot in serum from CDG Ia patients.
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0.9891 In contrast we were not able to detect hypoglycosylation in Proteinalpha1 - antitrypsin synthesized by fibroblasts, keratinocytes, enterocytes, and leukocytes.
0.8951 In contrast we were not able to detect Glycosylationhypoglycosylation in alpha1 - antitrypsin synthesized by fibroblasts, keratinocytes, enterocytes, and leukocytes.
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0.9983 Similarly no hypoglycosylation was detectable in a membrane - associated N - linked glycoprotein, the facilitative glucose transporter ProteinGLUT - 1 and also in serum immunoglobulin G isolated from sera of CDG Ia patients.
0.8071 Similarly no Glycosylationhypoglycosylation was detectable in a membrane - associated N - linked glycoprotein, the facilitative glucose transporter GLUT - 1 and also in serum immunoglobulin G isolated from sera of CDG Ia patients.
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0.9993 Molecular cloning and characterization of ProteinCHM1L , a novel membrane molecule similar to chondromodulin - I.
0.9965 Molecular cloning and characterization of CHM1L, a novel membrane molecule similar to Proteinchondromodulin - I .
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0.9790 Chondromodulin - I Protein( ChM - I ) is a cartilage - specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells.
0.9666 ProteinChondromodulin - I ( ChM - I ) is a cartilage - specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells.
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0.9996 In the present study, we identified a novel ChM - I like molecule, designated ProteinChM1L .
0.9846 In the present study, we identified a novel ProteinChM - I like molecule, designated ChM1L.
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0.9999 Cloning of full length cDNAs of human, mouse, and rat ProteinChM1L revealed that ChM1L encodes 317 amino acids novel type II transmembrane protein.
0.9998 Cloning of full length cDNAs of human, mouse, and rat ChM1L revealed that ProteinChM1L encodes 317 amino acids novel type II transmembrane protein.
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0.9980 ProteinChM1L protein was expressed on the cell surface as N - glycosylated and non - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively.
0.9895 ChM1L protein was expressed on the cell surface as GlycosylationN - glycosylated and non - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively.
0.9871 ChM1L protein was expressed on the cell surface as N - glycosylated and Glycosylationnon - N - glycosylated protein with molecular mass of 45 and 40 kDa, respectively.
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0.9993 In adult mouse tissues, ProteinChM1L mRNA was highly expressed in eye, skeletal muscle, and whole rib.
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0.9988 The temporal pattern of ProteinChM1L mRNA was examined using whole embryo at day 10 to 19 of gestation.
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0.9990 After day 11, ProteinChM1L mRNA was detected and its level was progressively elevated in association with development of mouse embryo.
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0.9998 These data suggest that ChM1L is a novel membrane molecule which is similar to ProteinChM - I that plays a regulatory role in eye, skeletal muscle, and development of embryo.
0.9992 These data suggest that ProteinChM1L is a novel membrane molecule which is similar to ChM - I that plays a regulatory role in eye, skeletal muscle, and development of embryo.
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0.9886 A chimeric CS - hemoagglutinin 1 ( HA1 ), obtained by adding the nine amino acid viral epitope Proteinhemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A.
0.9843 A chimeric CS - hemoagglutinin 1 Protein( HA1 ) , obtained by adding the nine amino acid viral epitope hemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A.
0.9049 A chimeric ProteinCS - hemoagglutinin 1 ( HA1 ), obtained by adding the nine amino acid viral epitope hemoagglutinin to the carboxy terminal of CS and shown to be correctly segregated to skeletal muscle jSR [ A.
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0.9976 To test this hypothesis, ProteinCS - HA1DeltaGly , a mutant in which the unique N - glycosylation site Asn316 was changed to Ile, was engineered by site - directed mutagenesis.
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0.9989 The expression and intracellular localization of ProteinCS - HA1DeltaGly was studied by double - labeling epifluorescence by means of antibodies against either CS, HA1, or the ryanodine receptor calcium release channel.
0.9979 The expression and intracellular localization of CS - HA1DeltaGly was studied by double - labeling epifluorescence by means of antibodies against either CS, ProteinHA1 , or the ryanodine receptor calcium release channel.
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0.9981 ProteinCS - HA1DeltaGly was expressed and retained to ER and ER / sarcoplasmic reticulum of HeLa cells and myotubes, respectively, and expressed, sorted, and correctly segregated to jSR of regenerating soleus muscle fibers.
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0.8673 Targeting of HIF - alpha to the Proteinvon Hippel - Lindau ubiquitylation complex by O2 - regulated prolyl hydroxylation.
0.6717 Targeting of HIF - alpha to the von ProteinHippel - Lindau ubiquitylation complex by O2 - regulated prolyl hydroxylation.
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0.9720 In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the von Hippel - Lindau tumor suppressor Protein( pVHL ) E3 ligase complex.
0.9280 In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the Proteinvon Hippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex.
0.8724 In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves ubiquitylation by the von ProteinHippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex.
0.8001 In oxygenated and iron replete cells, HIF - alpha subunits are rapidly destroyed by a mechanism that involves Ubiquitinationubiquitylation by the von Hippel - Lindau tumor suppressor ( pVHL ) E3 ligase complex.
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0.9977 Here we show that the interaction between human ProteinpVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ).
0.9930 Here we show that the interaction between human pVHL and a specific domain of the ProteinHIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ).
0.9523 Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue Protein( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ).
0.9316 Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through hydroxylation of a proline residue ( HIF - 1alpha EntityP564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ).
0.9171 Here we show that the interaction between human pVHL and a specific domain of the HIF - 1alpha subunit is regulated through Hydroxylationhydroxylation of a proline residue ( HIF - 1alpha P564 ) by an enzyme we have termed HIF - alpha prolyl - hydroxylase ( HIF - PH ).
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0.9980 HIFalpha targeted for ProteinVHL - mediated destruction by proline hydroxylation : implications for O2 sensing.
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0.9888 In the presence of oxygen, HIF is targeted for destruction by an E3 Proteinubiquitin ligase containing the von Hippel - Lindau tumor suppressor protein ( pVHL ).
0.9856 In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the von Hippel - Lindau tumor suppressor protein Protein( pVHL ) .
0.8214 In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the Proteinvon Hippel - Lindau tumor suppressor protein ( pVHL ).
0.6451 In the presence of oxygen, HIF is targeted for destruction by an E3 ubiquitin ligase containing the von ProteinHippel - Lindau tumor suppressor protein ( pVHL ).
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0.9990 We found that human ProteinpVHL binds to a short HIF - derived peptide when a conserved proline residue at the core of this peptide is hydroxylated.
0.7480 We found that human pVHL binds to a short HIF - derived peptide when a conserved proline residue at the core of this peptide is Hydroxylationhydroxylated .
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0.9946 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for Entitypromoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes.
0.9939 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, ProteinhMSH2 , hMSH3, and hMSH6 genes.
0.9931 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including ProteinhMLH1 , hMSH2, hMSH3, and hMSH6 genes.
0.9926 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, ProteinhMSH3 , and hMSH6 genes.
0.9919 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and ProteinhMSH6 genes.
0.9902 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for promoter DNA_methylationmethylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes.
0.6006 We analyzed 100 sporadic and 3 hereditary pancreatic ductal adenocarcinomas for MSI, and high - frequency MSI ( MSI - H ) and low - frequency MSI ( MSI - L ) tumors were further analyzed for frameshift mutations of possible target genes and for DNA_methylationpromoter methylation and mutation of DNA MMR genes, including hMLH1, hMSH2, hMSH3, and hMSH6 genes.
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0.9996 MSI - H tumors were significantly associated with poor differentiation and the presence of wild - type K - RAS and Proteinp53 genes.
0.9989 MSI - H tumors were significantly associated with poor differentiation and the presence of wild - type ProteinK - RAS and p53 genes.
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0.9990 Frameshift mutations of hMSH3, ProteinhMLH3 , BRCA - 2, TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors.
0.9989 Frameshift mutations of hMSH3, hMLH3, BRCA - 2, TGF - beta type II receptor, and ProteinBAX genes were detected in MSI - H tumors.
0.9988 Frameshift mutations of ProteinhMSH3 , hMLH3, BRCA - 2, TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors.
0.9721 Frameshift mutations of hMSH3, hMLH3, ProteinBRCA - 2 , TGF - beta type II receptor, and BAX genes were detected in MSI - H tumors.
0.8722 Frameshift mutations of hMSH3, hMLH3, BRCA - 2, ProteinTGF - beta type II receptor , and BAX genes were detected in MSI - H tumors.
0.7320 Frameshift mutations of hMSH3, hMLH3, BRCA - 2, TGF - beta Proteintype II receptor , and BAX genes were detected in MSI - H tumors.
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0.9899 DNA_methylationHypermethylation of the hMLH1 promoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors.
0.9869 Hypermethylation of the hMLH1 Entitypromoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors.
0.9686 Hypermethylation of the ProteinhMLH1 promoter was observed in 6 ( 46 % ) of the 13 sporadic MSI - H tumors but not in any of the 3 hereditary MSI - H tumors or 13 MSI - L tumors.
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0.9980 All of the 3 HNPCC cases had germ - line ProteinhMLH1 mutation accompanied by loss of heterogeneity or other mutation in the tumor.
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0.9994 Our results also suggest the principal involvement of epigenetic or genetic inactivation of the ProteinhMLH1 gene in the pathogenesis of pancreatic carcinoma with MSI - H.
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0.9931 The acetylation state of human fetal hemoglobin modulates the strength of its subunit interactions : long - range effects and implications for Proteinhistone interactions in the nucleosome.
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0.9895 Evidence for this conclusion was obtained by demonstrating that natural hemoglobin F ( 1 ), which is specifically Acetylationacetylated at Gly - 1 ( gamma ) and hence unable to be protonated, behaves like HbA and not HbF in its tetramer - dimer association properties over the pH range studied.
0.5746 Evidence for this conclusion was obtained by demonstrating that natural hemoglobin F ( 1 ), which is specifically acetylated at Gly - 1 ( gamma ) and hence unable to be protonated, behaves like HbA and not ProteinHbF in its tetramer - dimer association properties over the pH range studied.
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0.7990 An increased degree of protonation of the gamma - chain N - terminus of Proteinhemoglobin F from pH 9. 0 to 8. 0 is therefore suggested as responsible for its increased tetramer strength representing an example of transmission of a signal from its positively charged N - terminal tail to the distant subunit allosteric interface where the equilibrium constant is measured.
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0.9642 An analogy is made between the effects of acetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and acetylation of some internal Lys residues within the N - terminal segments of the Proteinhistone octamer around which DNA is wrapped in the nucleosome.
0.8934 An analogy is made between the effects of acetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and Acetylationacetylation of some internal Lys residues within the N - terminal segments of the histone octamer around which DNA is wrapped in the nucleosome.
0.8563 An analogy is made between the effects of Acetylationacetylation of the fetal hemoglobin tetramer on the strength of its subunit interactions and acetylation of some internal Lys residues within the N - terminal segments of the histone octamer around which DNA is wrapped in the nucleosome.
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0.9980 Synergism of ProteinXist RNA, DNA methylation, and histone hypoacetylation in maintaining X chromosome inactivation.
0.9979 Synergism of Xist RNA, DNA methylation, and Proteinhistone hypoacetylation in maintaining X chromosome inactivation.
0.9572 Synergism of Xist RNA, DNA methylation, and histone Acetylationhypoacetylation in maintaining X chromosome inactivation.
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0.9952 ProteinXist RNA expression, methylation of CpG islands, and hypoacetylation of histone H4 are distinguishing features of inactive X chromatin.
0.9492 Xist RNA expression, methylation of CpG islands, and Acetylationhypoacetylation of histone H4 are distinguishing features of inactive X chromatin.
0.9371 Xist RNA expression, methylation of CpG islands, and hypoacetylation of Proteinhistone H4 are distinguishing features of inactive X chromatin.
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0.9994 ProteinXist RNA has been shown to be essential for initiation of X inactivation, but not required for maintenance.
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0.9992 Using a conditional mutant ProteinXist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts.
0.9990 Using a conditional mutant Xist allele, we provide direct evidence for that loss of ProteinXist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts.
0.9937 Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked ProteinGFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts.
0.9802 Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine phosphoribosyl transferase Protein( Hprt ) gene in mouse embryonic fibroblasts.
0.7822 Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous Proteinhypoxanthine phosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts.
0.6631 Using a conditional mutant Xist allele, we provide direct evidence for that loss of Xist RNA destabilizes the inactive state in somatic cells, leading to an increased reactivation frequency of an X - linked GFP transgene and of the endogenous hypoxanthine Proteinphosphoribosyl transferase ( Hprt ) gene in mouse embryonic fibroblasts.
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0.9998 Demethylation of DNA, using 5 - azadC or by introducing a mutation in ProteinDnmt1 , and inhibition of histone hypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms.
0.9990 Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of histone hypoacetylation using trichostatin A further increases reactivation in ProteinXist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms.
0.9982 Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of Proteinhistone hypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms.
0.9328 Demethylation of DNA, using 5 - azadC or by introducing a mutation in Dnmt1, and inhibition of histone Acetylationhypoacetylation using trichostatin A further increases reactivation in Xist mutant fibroblasts, indicating a synergistic interaction of X chromosome silencing mechanisms.
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0.9876 Expression of Pichia anomala ProteinINV1 gene in Saccharomyces cerevisiae results in two different active forms of hypoglycosylated invertase.
0.9655 Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of hypoglycosylated Proteininvertase .
0.7915 Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase.
0.3612 Expression of Pichia anomala INV1 gene in Saccharomyces cerevisiae results in two different active forms of Glycosylationhypoglycosylated invertase .
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0.9959 The Pichia anomala invertase gene Protein( INV1 ) was introduced at different copy numbers into a sucrose - nonfermenting mutant of Saccharomyces cerevisiae and expressed from its own promoter sequences.
0.9814 The Pichia anomala Proteininvertase gene ( INV1 ) was introduced at different copy numbers into a sucrose - nonfermenting mutant of Saccharomyces cerevisiae and expressed from its own promoter sequences.
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0.9998 The level reached in the production of invertase by the transformants ( up to 540 units / 10 ( 10 ) cells ) was in agreement with the ProteinINV1 gene dosage.
0.9996 The level reached in the production of Proteininvertase by the transformants ( up to 540 units / 10 ( 10 ) cells ) was in agreement with the INV1 gene dosage.
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0.9991 Two forms of multimeric active and glycosylated Proteininvertase displaying different subcellular locations and molecular masses could be detected in the transformants.
0.9923 Two forms of multimeric active and Glycosylationglycosylated invertase displaying different subcellular locations and molecular masses could be detected in the transformants.
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0.9992 Each of the two heterologous forms of Proteininvertase was shown to be an oligomer composed of identical subunits.
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0.9700 The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their GlycosylationN - linked oligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms.
0.6540 The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their N - linked Entityoligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms.
0.8428 The difference found in the apparent molecular masses of their monomers ( 81. 5 and 78. 3 kDa, respectively ) seems to be due to the size of their N - linked Entityoligosaccharide chains ( on average 2. 4 and 1. 9 kDa, respectively ), since the number of sugar chains ( 9 ) and the molecular mass of the protein moiety ( 60. 5 kDa ) are identical in both forms.
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0.9991 The hypoglycosylated Proteininvertase accumulated within the cells of the transformants to an unusual level ( up to 130 units / 10 ( 10 ) cells ).
0.9436 The Glycosylationhypoglycosylated invertase accumulated within the cells of the transformants to an unusual level ( up to 130 units / 10 ( 10 ) cells ).
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0.9873 Such accumulation of active enzyme inside the cells, as well as its underglycosylation, could be due to intrinsic properties of the P. anomala Proteininvertase that are determined by the particular primary structure of its protein moiety.
0.8928 Such accumulation of active enzyme inside the cells, as well as its Glycosylationunderglycosylation , could be due to intrinsic properties of the P. anomala invertase that are determined by the particular primary structure of its protein moiety.
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0.9989 The histone acetyltransferase, ProteinhGCN5 , interacts with and acetylates the HIV transactivator, Tat.
0.9973 The histone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, ProteinTat .
0.9253 The Proteinhistone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, Tat.
0.6166 The histone acetyltransferase, hGCN5, interacts with and Acetylationacetylates the HIV transactivator, Tat.
The histone acetyltransferase, hGCN5, interacts with and Catalysisacetylates the HIV transactivator, Tat.
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0.9885 Factor acetyltransferase activity associated with several Proteinhistone acetyltransferases plays a key role in the control of transcription.
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0.9991 Here we report that ProteinhGCN5 , a well known histone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat.
0.9980 Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, ProteinTat .
0.9107 Here we report that hGCN5, a well known Proteinhistone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat.
0.6106 Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and Acetylationacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat.
Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and Catalysisacetylates the human immunodeficiency virus type 1 ( HIV - 1 ) transactivator protein, Tat.
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0.9997 The interaction between Tat and ProteinhGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of Tat encompassing the cysteine - rich domain of the protein.
0.9997 The interaction between Tat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of ProteinhGCN5 , as well as a limited region of Tat encompassing the cysteine - rich domain of the protein.
0.9996 The interaction between ProteinTat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of Tat encompassing the cysteine - rich domain of the protein.
0.9996 The interaction between Tat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of ProteinTat encompassing the cysteine - rich domain of the protein.
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0.9948 Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by ProteinhGCN5 .
0.9765 Tat lysines 50 and 51, target of acetylation by Proteinp300 / CBP , were also found to be acetylated by hGCN5.
0.9588 ProteinTat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5.
0.9549 Tat lysines 50 and 51, target of Acetylationacetylation by p300 / CBP, were also found to be acetylated by hGCN5.
0.9433 Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5.
0.9246 Tat lysines 50 and Entity51 , target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5.
0.7615 Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Acetylationacetylated by hGCN5.
0.6654 Tat Entitylysines 50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5.
0.5247 Tat lysines Entity50 and 51, target of acetylation by p300 / CBP, were also found to be acetylated by hGCN5.
Tat lysines 50 and 51, target of acetylation by p300 / CBP, were also found to be Catalysisacetylated by hGCN5.
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0.9970 The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that ProteinhGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat.
0.9952 The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance ProteinTat - dependent transcription of the HIV - 1 long terminal repeat.
0.9942 The acetylation of these two lysines by Proteinp300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat.
0.9940 The Acetylationacetylation of these two lysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat.
0.9935 The acetylation of these two lysines by p300 / CBP has been recently shown to stimulate ProteinTat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat.
0.9825 The acetylation of these two Entitylysines by p300 / CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat - dependent transcription of the HIV - 1 long terminal repeat.
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0.9933 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, ProteinGCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.9855 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of ProteinTat , since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.9854 These data highlight the importance of the Acetylationacetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.9808 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and Proteinp300 / CBP , converge to acetylate Tat on the same site.
0.9730 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different Proteinhistone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.9638 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate ProteinTat on the same site.
0.9603 These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.9145 These data highlight the importance of the acetylation of lysines 50 and Entity51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
0.6727 These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Acetylationacetylate Tat on the same site.
0.8143 These data highlight the importance of the acetylation of Entitylysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to acetylate Tat on the same site.
These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300 / CBP, converge to Catalysisacetylate Tat on the same site.
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0.9858 Hydroxylating activity of frog epidermis Proteintyrosinase .
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0.9951 Trypsin activated in a similar way both the tyrosine hydroxylase and the dopa - oxidasa activities of frog epidermis Proteintyrosinase .
0.9591 Trypsin activated in a similar way both the Proteintyrosine hydroxylase and the dopa - oxidasa activities of frog epidermis tyrosinase.
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0.9577 ProteinTyrosine hydroxylase had KM = 2. 6 X 10 ( - 3 ) M for tyrosine and 2 x 10 ( - 3 ) M dopa was a competitive inhibitor with Ki = 5 x 10 ( - 4 ) M.
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0.9957 Canine ProteinCOL1A2 mutation resulting in C - terminal truncation of pro - alpha2 ( I ) and severe osteogenesis imperfecta.
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0.9993 In a nonisotopic RNAse cleavage assay ( NIRCA ), the proband's RNA had a unique cleavage pattern in the region of ProteinCOL1A2 encoding the C - propeptide.
0.9987 In a nonisotopic RNAse cleavage assay ( NIRCA ), the proband's RNA had a unique cleavage pattern in the region of COL1A2 encoding the ProteinC - propeptide .
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0.9901 DNA sequence analyses identified a mutation in which nucleotides 3991 - 3994 ( " CTAG " ) were replaced with " TGTCATTGG. " The first seven bases of the inserted sequence were identical to nucleotides 4002 - 4008 of the normal canine ProteinCOL1A2 sequence.
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0.9980 Increased density of ProteinpC - alpha2 ( I ) suggested comigration with the similarly sized pro - alpha2 ( I ) derived from the mutant allele.
0.9897 Increased density of pC - alpha2 ( I ) suggested comigration with the similarly sized Proteinpro - alpha2 ( I ) derived from the mutant allele.
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0.9948 Furthermore, a - chains were overhydroxylated and the ratio of Proteinalpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of alpha1 ( I ) homotrimers.
0.9905 Furthermore, a - chains were overhydroxylated and the ratio of alpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of Proteinalpha1 ( I ) homotrimers.
0.2319 Furthermore, a - chains were Hydroxylationoverhydroxylated and the ratio of alpha1 ( I ) : alpha2 ( I ) was 3. 2 : 1, consistent with the presence of alpha1 ( I ) homotrimers.
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0.9992 Analyses of ProteinCOL1A2 and type I collagen were both consistent with the described heterozygous mutation affecting the pro - alpha2 ( I ) C - propeptide and confirmed a diagnosis of OI.
0.9913 Analyses of COL1A2 and type I collagen were both consistent with the described heterozygous mutation affecting the Proteinpro - alpha2 ( I ) C - propeptide and confirmed a diagnosis of OI.
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0.9969 Linking global Proteinhistone acetylation to the transcription enhancement of X - chromosomal genes in Drosophila males.
0.9966 Linking global histone Acetylationacetylation to the transcription enhancement of X - chromosomal genes in Drosophila males.
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0.9966 It has become well established for several genes that targeting of Proteinhistone acetylation to promoters is required for the activation of transcription.
0.9949 It has become well established for several genes that targeting of histone Acetylationacetylation to promoters is required for the activation of transcription.
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0.9376 In contrast, global patterns of Acetylationacetylation have not been ascribed to any particular regulatory function.
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0.9982 In Drosophila, a specific modification of ProteinH4 , acetylation at lysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex.
0.9936 In Drosophila, a specific modification of H4, Acetylationacetylation at lysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex.
0.9415 In Drosophila, a specific modification of H4, acetylation at Entitylysine 16 , is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex.
0.5570 In Drosophila, a specific modification of H4, acetylation at Entitylysine 16, is enriched at hundreds of sites on the male X chromosome due to the activity of the male - specific lethal ( MSL ) dosage compensation complex.
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0.9858 Utilizing chromatin immunoprecipitation, we have determined that H4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of Acetylationacetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units.
0.9683 Utilizing chromatin immunoprecipitation, we have determined that ProteinH4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of acetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units.
Utilizing chromatin immunoprecipitation, we have determined that EntityH4Ac16 is present along the entire length of X - linked genes targeted by the MSL complex with relatively modest levels of acetylation at the promoter regions and high levels in the middle and / or 3'end of the transcription units.
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0.9508 We propose that global Acetylationacetylation by the MSL complex increases the expression of X - linked genes by facilitating transcription elongation rather than by enhancing promoter accessibility.
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0.9967 We have also determined that ProteinH4Ac16 is absent from a region of the X chromosome that includes a gene known to be dosage - compensated by a MSL - independent mechanism.
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0.9937 Correlation between histone lysine methylation and developmental changes at the chicken Proteinbeta - globin locus.
0.9655 Correlation between Proteinhistone lysine methylation and developmental changes at the chicken beta - globin locus.
0.9525 Correlation between histone lysine Methylationmethylation and developmental changes at the chicken beta - globin locus.
0.9095 Correlation between histone Entitylysine methylation and developmental changes at the chicken beta - globin locus.
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0.9852 Methylation of Proteinhistones at specific residues plays an important role in transcriptional regulation.
0.9722 MethylationMethylation of histones at specific residues plays an important role in transcriptional regulation.
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0.9962 Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken Proteinbeta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation.
0.9866 Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 Methylationmethylation and acetylation.
0.9472 Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated Entitylysine 9 methylation and acetylation.
0.8892 Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and Acetylationacetylation .
0.8396 Chromatin immunoprecipitation of dimethylated lysine 9 on Proteinhistone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation.
0.7354 Chromatin immunoprecipitation of Methylationdimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation.
0.7054 Chromatin immunoprecipitation of dimethylated Entitylysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated lysine 9 methylation and acetylation.
0.7563 Chromatin immunoprecipitation of dimethylated lysine 9 on histone H3 across 53 kilobases of the chicken beta - globin locus during erythropoiesis shows an almost complete anticorrelation between regions of elevated Entitylysine 9 methylation and acetylation.
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0.9681 Lysine 9 is Methylationmethylated most over constitutive condensed chromatin and developmentally inactive globin genes.
0.8260 EntityLysine 9 is methylated most over constitutive condensed chromatin and developmentally inactive globin genes.
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0.9724 In contrast, lysine 4 methylation of histone H3 correlates with H3 Acetylationacetylation .
0.9719 In contrast, lysine 4 methylation of histone H3 correlates with ProteinH3 acetylation.
0.9194 In contrast, lysine 4 methylation of Proteinhistone H3 correlates with H3 acetylation.
0.8455 In contrast, lysine 4 Methylationmethylation of histone H3 correlates with H3 acetylation.
In contrast, Entitylysine 4 methylation of histone H3 correlates with H3 acetylation.
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0.9923 These results lead us to propose a mechanism by which the insulator in the Proteinbeta - globin locus can protect the globin genes from being silenced by adjacent condensed chromatin.
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0.9753 Purification and characterization of a soluble bioactive amino - terminal extracellular domain of the human Proteinthyrotropin receptor .
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0.9469 The amino - terminal ectodomain of the human ProteinTSH receptor has been expressed at the surface of CHO cells as a glycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus.
0.7491 The amino - terminal ectodomain of the human TSH receptor has been expressed at the surface of CHO cells as a Glycosylationglycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus.
The amino - terminal ectodomain of the human TSH receptor has been expressed at the surface of CHO cells as a Entityglycosylphosphatidylinositol - anchored molecule containing a 10 - residue histidine tag close to its C terminus.
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0.8493 The soluble ectodomain could be released from the cells by treatment with a Proteinglycosylphosphatidylinositol - phospholipase C and purified to apparent homogeneity by cobalt - Sepharose chromatography.
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0.9916 This allowed the identification of four out of the six potential N - glycosylation sites as being effectively Glycosylationglycosylated .
0.7807 This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively glycosylated.
0.6101 This allowed the identification of four out of the six potential EntityN - glycosylation sites as being effectively glycosylated.
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0.9913 A proportion of the purified soluble ectodomain displayed specific binding of ( 125 ) I - labeled ProteinTSH , allowing for the first time performance of classical saturation binding experiments.
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0.9976 Contrary to all currently available assays, the soluble ectodomain of the TSH receptor purified in a functionally competent conformation allows direct studies of its interactions with ProteinTSH and autoantibodies and opens the way to structural studies.
0.9790 Contrary to all currently available assays, the soluble ectodomain of the ProteinTSH receptor purified in a functionally competent conformation allows direct studies of its interactions with TSH and autoantibodies and opens the way to structural studies.
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0.9988 ProteinHIF - 1alpha binding to VHL is regulated by stimulus - sensitive proline hydroxylation.
0.9982 HIF - 1alpha binding to ProteinVHL is regulated by stimulus - sensitive proline hydroxylation.
0.9823 HIF - 1alpha binding to VHL is regulated by stimulus - sensitive Entityproline hydroxylation.
0.9502 HIF - 1alpha binding to VHL is regulated by stimulus - sensitive proline Hydroxylationhydroxylation .
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0.9507 Hypoxia - inducible factor - 1alpha Protein( HIF - 1alpha ) is a global transcriptional regulator of the hypoxic response.
0.7768 ProteinHypoxia - inducible factor - 1alpha ( HIF - 1alpha ) is a global transcriptional regulator of the hypoxic response.
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0.9971 Under normoxic conditions, ProteinHIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex.
0.9899 Under normoxic conditions, HIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 Proteinubiquitin ligase complex.
0.9859 Under normoxic conditions, HIF - 1alpha is recognized by the von Hippel - Lindau tumor - suppressor protein Protein( VHL ) , a component of an E3 ubiquitin ligase complex.
0.7529 Under normoxic conditions, HIF - 1alpha is recognized by the Proteinvon Hippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex.
0.5662 Under normoxic conditions, HIF - 1alpha is recognized by the von ProteinHippel - Lindau tumor - suppressor protein ( VHL ), a component of an E3 ubiquitin ligase complex.
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0.9990 This interaction thereby promotes the rapid degradation of ProteinHIF - 1alpha .
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0.9985 Under hypoxic conditions, ProteinHIF - 1alpha is stabilized.
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0.9994 We have previously shown that ProteinVHL binds in a hypoxia - sensitive manner to a 27 - aa segment of HIF - 1alpha, and that this regulation depends on a posttranslational modification of HIF - 1alpha.
0.9988 We have previously shown that VHL binds in a hypoxia - sensitive manner to a 27 - aa segment of HIF - 1alpha, and that this regulation depends on a posttranslational modification of ProteinHIF - 1alpha .
0.9987 We have previously shown that VHL binds in a hypoxia - sensitive manner to a 27 - aa segment of ProteinHIF - 1alpha , and that this regulation depends on a posttranslational modification of HIF - 1alpha.
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0.9974 Through a combination of in vivo coimmunoprecipitation assays using ProteinVHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of HIF - 1alpha.
0.9960 Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of ProteinHIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of HIF - 1alpha.
0.9951 Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of Pro - 564 of ProteinHIF - 1alpha .
0.9949 Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is hydroxylation of EntityPro - 564 of HIF - 1alpha.
0.9673 Through a combination of in vivo coimmunoprecipitation assays using VHL and a panel of point mutants of HIF - 1alpha in this region, as well as MS and in vitro binding assays, we now provide evidence that this modification, which occurs under normoxic conditions, is Hydroxylationhydroxylation of Pro - 564 of HIF - 1alpha.
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0.9959 The data furthermore show that this proline hydroxylation is the primary regulator of ProteinVHL binding.
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0.9992 2B4 ( CD244 ) and CS1 : novel members of the ProteinCD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes.
0.9981 2B4 ( CD244 ) and ProteinCS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes.
0.9837 Protein2B4 ( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes.
0.8892 2B4 Protein( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes.
0.6130 Protein2B4 ( CD244 ) and CS1 : novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes.
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0.9994 Protein2B4 is a member of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer ( NK ) cells and other leukocytes.
0.9990 2B4 is a member of the ProteinCD2 subset of the immunoglobulin superfamily molecules expressed on natural killer ( NK ) cells and other leukocytes.
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0.9989 It is the high affinity ligand for ProteinCD48 .
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0.9989 Engagement of 2B4 on NK - cell surfaces with specific antibodies or ProteinCD48 can trigger cell - mediated cytotoxicity, interferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness.
0.9989 Engagement of Protein2B4 on NK - cell surfaces with specific antibodies or CD48 can trigger cell - mediated cytotoxicity, interferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness.
0.9979 Engagement of 2B4 on NK - cell surfaces with specific antibodies or CD48 can trigger cell - mediated cytotoxicity, Proteininterferon - gamma secretion, phosphoinositol turnover and NK - cell invasiveness.
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0.9997 The function of 2B4 in ProteinCD8 + T cells and myeloid cells remains unknown.
0.9988 The function of Protein2B4 in CD8 + T cells and myeloid cells remains unknown.
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0.9992 The cytoplasmic domain of Protein2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with src homology 2 domain - containing protein or signaling lymphocyte activation molecule ( SLAM ) - associated protein, whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ).
0.6419 The cytoplasmic domain of 2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with Proteinsrc homology 2 domain - containing protein or signaling lymphocyte activation molecule ( SLAM ) - associated protein, whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ).
The cytoplasmic domain of 2B4 contains unique tyrosine motifs ( TxYxxV / I ) that associate with src homology 2 domain - containing protein or Proteinsignaling lymphocyte activation molecule ( SLAM ) - associated protein , whose mutation is the underlying genetic defect in the X - linked lymphoproliferative disease ( XLPD ).
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0.9798 Impaired signaling via Protein2B4 and SLAM is implicated in the immunopathogenesis of XLPD.
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0.9996 CS1 is a novel member of the ProteinCD2 subset that contains two of the unique tyrosine motifs present in 2B4 and SLAM.
0.9994 ProteinCS1 is a novel member of the CD2 subset that contains two of the unique tyrosine motifs present in 2B4 and SLAM.
0.9895 CS1 is a novel member of the CD2 subset that contains two of the unique tyrosine motifs present in Protein2B4 and SLAM.
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0.9995 Signaling through 2B4, CS1 and other members of the ProteinCD2 subset may play a major role in the regulation of NK cells and other leukocyte functions.
0.9994 Signaling through 2B4, ProteinCS1 and other members of the CD2 subset may play a major role in the regulation of NK cells and other leukocyte functions.
0.9982 Signaling through Protein2B4 , CS1 and other members of the CD2 subset may play a major role in the regulation of NK cells and other leukocyte functions.
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0.9840 GlycosylationN - glycosylation of CRF receptor type 1 is important for its ligand - specific interaction.
0.8376 N - glycosylation of ProteinCRF receptor type 1 is important for its ligand - specific interaction.
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0.9446 The corticotropin - releasing factor ( CRF ) receptor type 1 Protein( CRFR1 ) contains five potential N - glycosylation sites : N38, N45, N78, N90, and N98.
The Proteincorticotropin - releasing factor ( CRF ) receptor type 1 ( CRFR1 ) contains five potential N - glycosylation sites : N38, N45, N78, N90, and N98.
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0.9994 Cells expressing ProteinCRFR1 were treated with tunicamycin to block receptor glycosylation.
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0.9989 The nonglycosylated receptor did not bind the radioligand and had a decreased cAMP stimulation potency in response to ProteinCRF .
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0.9935 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound ProteinCRF , sauvagine ( SVG ), and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.9903 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and Proteinurotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.9861 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and urotensin - I Protein( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.9698 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine Protein( SVG ) , and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.9151 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, Proteinsauvagine ( SVG ), and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.6232 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, sauvagine ( SVG ), and Proteinurotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
0.6147 The single mutants Q38, Q45, Q78, Q90, Q98, A40, A47, A80, A92, and A100 and the double mutants A40 / A47 and A80 / A100 were well expressed, bound CRF, Proteinsauvagine ( SVG ) , and urotensin - I ( UTS - I ) with a normal affinity, and increased cAMP accumulation with a high efficiency.
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0.9998 These data indicate the requirement for three or more polysaccharide chains for normal ProteinCRFR1 function.
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0.9998 Reduced rates of gene loss, gene silencing, and gene mutation in ProteinDnmt1 - deficient embryonic stem cells.
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0.9998 In addition, we targeted the major DNA methyltransferase gene, ProteinDnmt1 , to investigate the relative contribution of DNA methylation to these various competing gene inactivation pathways.
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0.9993 Our data show that gene loss is the predominant mode of inactivation of a herpes simplex virus thymidine kinase neomycin phosphotransferase reporter gene ( HSV - TKNeo ) at the two integration sites tested and that this event is significantly reduced in ProteinDnmt1 - deficient cells.
0.5653 Our data show that gene loss is the predominant mode of inactivation of a herpes simplex virus Proteinthymidine kinase neomycin phosphotransferase reporter gene ( HSV - TKNeo ) at the two integration sites tested and that this event is significantly reduced in Dnmt1 - deficient cells.
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0.9998 Gene silencing by promoter methylation requires ProteinDnmt1 , suggesting that the expression of Dnmt3a and Dnmt3b alone in ES cells is insufficient to achieve effective gene silencing.
0.9997 Gene silencing by promoter methylation requires Dnmt1, suggesting that the expression of ProteinDnmt3a and Dnmt3b alone in ES cells is insufficient to achieve effective gene silencing.
0.9997 Gene silencing by promoter methylation requires Dnmt1, suggesting that the expression of Dnmt3a and ProteinDnmt3b alone in ES cells is insufficient to achieve effective gene silencing.
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0.9998 We used a novel assay to show that missense mutation rates are also substantially reduced in ProteinDnmt1 - deficient cells.
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0.9996 Surprisingly, the fraction of CpG transition mutations was not reduced in ProteinDnmt1 - deficient cells.
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0.9997 Finally, we show that methyl group - deficient growth conditions do not cause an increase in missense mutation rates in ProteinDnmt1 - proficient cells, as predicted by methyltransferase - mediated mutagenesis models.
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0.9999 We conclude that ProteinDnmt1 deficiency and the accompanying genomic DNA hypomethylation result in a reduction of three major pathways of gene inactivation in our model system.
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0.9987 Induction of hepatitis C virus ProteinE1 envelope protein - specific immune response can be enhanced by mutation of N - glycosylation sites.
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0.9986 We investigated the role played by N - glycans in the immunogenicity of hepatitis C virus ( HCV ) ProteinE1 envelope glycoprotein, a naturally poor immunogen.
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0.9996 Eight plasmids were engineered, encoding ProteinE1 protein mutants in which the four N - linked glycosylation sites of the protein were mutated separately or in combination.
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0.6787 In vitro expression studies showed an influence of GlycosylationN - linked glycosylation on expression efficiency, instability, and / or secretion of the mutated proteins.
0.7581 In vitro expression studies showed an influence of N - linked Glycosylationglycosylation on expression efficiency, instability, and / or secretion of the mutated proteins.
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0.9995 Immunogenicity of the ProteinE1 mutants was studied in BALB / c mice following intramuscular and intraepidermal injection of the plasmids.
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0.9989 Whereas some mutations had no or only minor effects on the antibody titers induced, mutation of the fourth glycosylation site ( N4 ) significantly enhanced the Proteinanti - E1 humoral response in terms of both seroconversion rates and antibody titers.
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0.9996 Epitope mapping indicated that the ProteinE1 mutant antigens induced antibody directed at two major domains : one, located at amino acids ( aa ) 313 to 332, which is known to be reactive with sera from HCV patients, and a second one, located in the N - terminal domain of E1 ( aa 192 to 226 ).
0.9969 Epitope mapping indicated that the E1 mutant antigens induced antibody directed at two major domains : one, located at amino acids ( aa ) 313 to 332, which is known to be reactive with sera from HCV patients, and a second one, located in the N - terminal domain of ProteinE1 ( aa 192 to 226 ).
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0.9356 Analysis of the induced immune cellular response confirmed the induction of Proteingamma interferon - producing cells by all mutants, albeit to different levels.
0.7378 Analysis of the induced immune cellular response confirmed the induction of gamma Proteininterferon - producing cells by all mutants, albeit to different levels.
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0.9993 These results show that N - linked glycosylation can limit the antibody response to the HCV ProteinE1 protein and reveal a potential vaccine candidate with enhanced immunogenicity.
0.9191 These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity.
0.9275 These results show that N - linked Glycosylationglycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity.
0.7148 These results show that GlycosylationN - linked glycosylation can limit the antibody response to the HCV E1 protein and reveal a potential vaccine candidate with enhanced immunogenicity.
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0.9993 The BAH genomic locus encodes three distinct proteins : Proteinjunctin , humbug, and BAH.
0.9993 The BAH genomic locus encodes three distinct proteins : junctin, humbug, and ProteinBAH .
0.9988 The ProteinBAH genomic locus encodes three distinct proteins : junctin, humbug, and BAH.
0.9987 The BAH genomic locus encodes three distinct proteins : junctin, Proteinhumbug , and BAH.
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0.9995 The biological roles of ProteinBAH and humbug and their functional relationship to junctin remain unclear.
0.9990 The biological roles of BAH and humbug and their functional relationship to Proteinjunctin remain unclear.
0.9990 The biological roles of BAH and Proteinhumbug and their functional relationship to junctin remain unclear.
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0.9996 To evaluate the role of ProteinBAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed.
0.9995 To evaluate the role of BAH in vivo, the catalytic domain of ProteinBAH was specifically targeted such that the coding regions of junctin and humbug remained undisturbed.
0.9993 To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of junctin and Proteinhumbug remained undisturbed.
0.9990 To evaluate the role of BAH in vivo, the catalytic domain of BAH was specifically targeted such that the coding regions of Proteinjunctin and humbug remained undisturbed.
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0.9816 BAH null mice lack measurable ProteinBAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X.
0.9787 ProteinBAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X.
0.9504 BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no Hydroxylationhydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X.
0.9359 BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting ProteinFactor X .
0.6169 BAH null mice lack measurable BAH protein in several tissues, lack Proteinaspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the epidermal growth factor ( EGF ) domain of clotting Factor X.
BAH null mice lack measurable BAH protein in several tissues, lack aspartyl beta - hydroxylase activity in liver preparations, and exhibit no hydroxylation of the Entityepidermal growth factor ( EGF ) domain of clotting Factor X.
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0.9995 In addition to reduced fertility in females, ProteinBAH null mice display several developmental defects including syndactyly, facial dysmorphology, and a mild defect in hard palate formation.
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0.9982 The developmental defects present in ProteinBAH null mice are similar to defects observed in knock - outs and hypomorphs of the Notch ligand Serrate - 2.
0.9975 The developmental defects present in BAH null mice are similar to defects observed in knock - outs and hypomorphs of the Notch ligand ProteinSerrate - 2 .
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0.9909 In this work, beta - hydroxylation of Asp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human ProteinJagged - 1 .
0.9170 In this work, Hydroxylationbeta - hydroxylation of Asp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1.
0.8369 In this work, beta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1.
0.5882 In this work, beta - hydroxylation of EntityAsp residues in EGF domains is demonstrated for a soluble form of a Notch ligand, human Jagged - 1.
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0.9990 Previous work has demonstrated increased levels of ProteinBAH in certain tumor tissues and a role for BAH in tumorigenesis has been proposed.
0.9985 Previous work has demonstrated increased levels of BAH in certain tumor tissues and a role for ProteinBAH in tumorigenesis has been proposed.
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0.9690 The role of hydroxylase in tumor formation was tested directly by crossing ProteinBAH KO mice with an intestinal tumor model, APCmin mice.
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0.9996 Surprisingly, ProteinBAH null / APCmin mice show a statistically significant increase in both intestinal polyp size and number when compared with BAH wild - type / APCmin controls.
0.9988 Surprisingly, BAH null / APCmin mice show a statistically significant increase in both intestinal polyp size and number when compared with ProteinBAH wild - type / APCmin controls.
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0.9989 These results suggest that, in contrast to expectations, loss of ProteinBAH catalytic activity may promote tumor formation.
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0.9986 Molecular cloning of ProteinESET , a novel histone H3 - specific methyltransferase that interacts with ERG transcription factor.
0.9966 Molecular cloning of ESET, a novel histone H3 - specific methyltransferase that interacts with ProteinERG transcription factor.
0.9323 Molecular cloning of ESET, a novel Proteinhistone H3 - specific methyltransferase that interacts with ERG transcription factor.
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0.9999 The ets - related gene Proteinerg encodes a transcription factor that is implicated in the control of cell growth and differentiation.
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0.9998 To identify interacting partners of ERG, we screened a yeast two - hybrid cDNA library constructed from mouse hematopoietic cells using the N - terminal region of ProteinERG as a bait.
0.9998 To identify interacting partners of ProteinERG , we screened a yeast two - hybrid cDNA library constructed from mouse hematopoietic cells using the N - terminal region of ERG as a bait.
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0.9931 We isolated a 4. 6 kb full - length mouse cDNA encoding a 1307 - amino acid protein migrating as a 180 kD band, which was termed ProteinESET ( ERG - associated protein with SET domain ).
We isolated a 4. 6 kb full - length mouse cDNA encoding a 1307 - amino acid protein migrating as a 180 kD band, which was termed ESET Protein( ERG - associated protein with SET domain ) .
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0.9991 ProteinESET is 92 % identical to the human protein SETDB1 ( SET domain, bifurcated 1 ).
0.9771 ESET is 92 % identical to the human protein ProteinSETDB1 ( SET domain, bifurcated 1 ).
ESET is 92 % identical to the human protein SETDB1 Protein( SET domain, bifurcated 1 ) .
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0.9998 The interaction between ESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous ProteinSETDB1 with ERG.
0.9998 The interaction between ESET and ProteinERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG.
0.9998 The interaction between ESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ProteinERG .
0.9997 The interaction between ProteinESET and ERG was supported by in vitro pull - down using glutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG.
0.6251 The interaction between ESET and ERG was supported by in vitro pull - down using Proteinglutathione S - transferase ( GST ) fusion protein, by transfection and co - immunoprecipitation experiments, and by association of endogenous SETDB1 with ERG.
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0.9988 Since ProteinESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to methylate core histones.
0.9986 Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ProteinESET to methylate core histones.
0.9815 Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to methylate core Proteinhistones .
0.9770 Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in Proteinhistone methylation, we tested the ability of ESET to methylate core histones.
0.9692 Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone Methylationmethylation , we tested the ability of ESET to methylate core histones.
0.8421 Since ESET possesses evolutionarily conserved SET, preSET, and postSET domains implicated in histone methylation, we tested the ability of ESET to Methylationmethylate core histones.
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0.9994 The results of these studies demonstrated that ProteinESET is a histone H3 - specific methyltransferase, and that mutations within ESET abolished its methyltransferase activity.
0.9993 The results of these studies demonstrated that ESET is a histone H3 - specific methyltransferase, and that mutations within ProteinESET abolished its methyltransferase activity.
0.9535 The results of these studies demonstrated that ESET is a Proteinhistone H3 - specific methyltransferase, and that mutations within ESET abolished its methyltransferase activity.
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0.9992 Together, these findings raise the possibility that transcription factor ProteinERG may participate in transcriptional regulation through ESET - mediated histone methylation.
0.9505 Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ESET - mediated histone Methylationmethylation .
0.6013 Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone methylation.
0.4680 Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ProteinESET - mediated histone methylation.
Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through ESET - mediated Proteinhistone methylation.
Together, these findings raise the possibility that transcription factor ERG may participate in transcriptional regulation through CatalysisESET - mediated histone methylation.
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0.8033 Regulation of HIF by the Proteinvon Hippel - Lindau tumour suppressor : implications for cellular oxygen sensing.
0.5814 Regulation of HIF by the von ProteinHippel - Lindau tumour suppressor : implications for cellular oxygen sensing.
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0.9990 A key insight has been the recognition that HIF - alpha is targeted for degradation by the Proteinubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha.
0.9953 A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 Proteinubiquitin ligase complex leading to ubiquitylation of HIF - alpha.
0.9911 A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein Protein( pVHL ) , which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha.
0.8337 A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the Proteinvon Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha.
0.9391 A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von Hippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to Ubiquitinationubiquitylation of HIF - alpha.
0.6917 A key insight has been the recognition that HIF - alpha is targeted for degradation by the ubiquitin - proteasome pathway through binding to the von ProteinHippel - Lindau tumour suppressor protein ( pVHL ), which forms the recognition component of an E3 ubiquitin ligase complex leading to ubiquitylation of HIF - alpha.
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0.9892 Importantly, the classical features of regulation by iron and oxygen availability are reflected in regulation of the ProteinHIF - alpha / pVHL interaction.
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0.9975 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with ProteinpVHL , and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro 564 ).
0.9639 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in Hydroxylationhydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro 564 ).
0.8824 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ).
0.8342 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue Protein( HIF - 1alpha , Pro 564 ).
0.5357 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, EntityPro 564 ) .
0.6449 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one Entityprolyl residue ( HIF - 1alpha, Pro 564 ).
0.5868 It has recently been shown that HIF - alpha undergoes an iron - and oxygen - dependent modification before it can interact with pVHL, and that this results in hydroxylation of at least one prolyl residue ( HIF - 1alpha, Pro Entity564 ) .
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0.5810 This modification is catalysed by an enzyme termed ProteinHIF - prolyl hydroxylase ( HIF - PH ), and compatible with all previously described prolyl - 4 - hydroxylases HIF - PH also requires 2 - oxoglutarate as a cosubstrate.
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0.6904 The key position of this Hydroxylationhydroxylation in the degradation pathway of HIF - alpha, together with its requirement for molecular dioxygen as a co - substrate, provides the potential for HIF - PH to function directly as a cellular oxygen sensor.
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0.9876 Promoter DNA_methylationmethylation status of the DNA repair genes hMLH1 and MGMT in gastric carcinoma and metaplastic mucosa.
0.9793 Promoter methylation status of the DNA repair genes ProteinhMLH1 and MGMT in gastric carcinoma and metaplastic mucosa.
0.9762 EntityPromoter methylation status of the DNA repair genes hMLH1 and MGMT in gastric carcinoma and metaplastic mucosa.
0.9760 Promoter methylation status of the DNA repair genes hMLH1 and ProteinMGMT in gastric carcinoma and metaplastic mucosa.
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0.9822 DNA repair genes human Mut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be DNA_methylationhypermethylated in certain carcinomas.
0.9377 DNA repair genes human Mut L homologue 1 Protein( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas.
0.9351 DNA repair genes human Mut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase Protein( MGMT ) have been shown to be hypermethylated in certain carcinomas.
0.9225 DNA repair genes human Mut L homologue 1 ( hMLH1 ) and ProteinO ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas.
0.8682 DNA repair genes human ProteinMut L homologue 1 ( hMLH1 ) and O ( 6 ) - methylguanine - DNA methyltransferase ( MGMT ) have been shown to be hypermethylated in certain carcinomas.
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0.9966 We studied DNA methylation of CpG islands in hMLH1 and ProteinMGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
0.9955 We studied DNA methylation of CpG islands in ProteinhMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
0.8821 We studied DNA_methylationDNA methylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
0.6843 We studied DNA methylation of EntityCpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
0.9370 We studied DNA DNA_methylationmethylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
0.6879 We studied DNA_methylationDNA methylation of CpG islands in hMLH1 and MGMT in 50 gastric carcinomas and 10 intestinal metaplastic mucosa samples.
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0.9992 We analyzed the methylation status of hMLH1 and ProteinMGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis.
0.9984 We analyzed the methylation status of ProteinhMLH1 and MGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis.
0.7930 We analyzed the DNA_methylationmethylation status of hMLH1 and MGMT using methylation - specific polymerase chain reaction and DNA sequencing analysis.
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0.9992 We measured protein levels of ProteinhMLH1 using Western blot and immunohistochemical analysis.
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0.9871 CpG island hypermethylation of hMLH1 and ProteinMGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively.
0.9736 CpG island hypermethylation of ProteinhMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively.
0.9541 CpG island DNA_methylationhypermethylation of hMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively.
0.8572 EntityCpG island hypermethylation of hMLH1 and MGMT was detected in 11 ( 22 % ) and 8 ( 16 % ) of the 50 gastric tumors, respectively.
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0.9800 DNA_methylationHypermethylation of the promoter was more common in intestinal - type gastric carcinomas than in poorly diffuse - type gastric carcinomas ( p = 0. 016 and 0. 021, respectively ; Fisher's exact test ).
0.9627 Hypermethylation of the Entitypromoter was more common in intestinal - type gastric carcinomas than in poorly diffuse - type gastric carcinomas ( p = 0. 016 and 0. 021, respectively ; Fisher's exact test ).
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0.9840 However, hMLH1 promoter DNA_methylationhypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient.
0.9765 However, hMLH1 promoter hypermethylation did not coincide with ProteinMGMT promoter hypermethylation except in 1 patient.
0.9746 However, hMLH1 promoter hypermethylation did not coincide with MGMT promoter DNA_methylationhypermethylation except in 1 patient.
0.9677 However, ProteinhMLH1 promoter hypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient.
0.9603 However, hMLH1 Entitypromoter hypermethylation did not coincide with MGMT promoter hypermethylation except in 1 patient.
0.9508 However, hMLH1 promoter hypermethylation did not coincide with MGMT Entitypromoter hypermethylation except in 1 patient.
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0.9816 DNA_methylationHypermethylation of the hMLH1 promoter but not the MGMT promoter occurred in intestinal metaplastic mucosae.
0.9754 Hypermethylation of the hMLH1 promoter but not the MGMT Entitypromoter occurred in intestinal metaplastic mucosae.
0.9646 Hypermethylation of the hMLH1 Entitypromoter but not the MGMT promoter occurred in intestinal metaplastic mucosae.
0.9570 Hypermethylation of the ProteinhMLH1 promoter but not the MGMT promoter occurred in intestinal metaplastic mucosae.
0.9513 Hypermethylation of the hMLH1 promoter but not the ProteinMGMT promoter occurred in intestinal metaplastic mucosae.
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0.9961 Immunohistochemical analysis revealed a corresponding reduction in ProteinhMLH1 protein expression in some of the intestinal metaplastic mucosae.
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0.5066 Our results suggest that at least two types of promoter DNA_methylationmethylation participate in the development of gastric carcinoma.
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0.9868 Tumor - specific promoter DNA_methylationhypermethylation of hMLH1 may be an early event in carcinogenesis in the stomach.
0.9857 Tumor - specific promoter hypermethylation of ProteinhMLH1 may be an early event in carcinogenesis in the stomach.
0.9539 Tumor - specific Entitypromoter hypermethylation of hMLH1 may be an early event in carcinogenesis in the stomach.
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0.9987 ProteinHistone deacetylases and cancer : causes and therapies.
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0.9995 Together, Proteinhistone acetyltransferases and histone deacetylases ( HDACs ) determine the acetylation status of histones.
0.9993 Together, histone acetyltransferases and Proteinhistone deacetylases ( HDACs ) determine the acetylation status of histones.
0.9944 Together, histone acetyltransferases and histone deacetylases ( HDACs ) determine the acetylation status of Proteinhistones .
0.9809 Together, histone acetyltransferases and histone deacetylases ( HDACs ) determine the Acetylationacetylation status of histones.
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0.9544 This Acetylationacetylation affects the regulation of gene expression, and inhibitors of HDACs have been found to cause growth arrest, differentiation and / or apoptosis of many tumours cells by altering the transcription of a small number of genes.
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0.9634 Co - and posttranslational modification of the Proteinalpha ( 1B ) - adrenergic receptor : effects on receptor expression and function.
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0.9103 We have characterized the maturation, co - and posttranslational modifications, and functional properties of the Proteinalpha ( 1B ) - adrenergic receptor ( AR ) expressed in different mammalian cells transfected using conventional approaches or the Semliki Forest virus system.
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0.9976 We found that the Proteinalpha ( 1B ) - AR undergoes N - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation.
0.9517 We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation.
0.9726 We found that the alpha ( 1B ) - AR undergoes N - linked Glycosylationglycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation.
0.7185 We found that the alpha ( 1B ) - AR undergoes GlycosylationN - linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation.
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0.9949 Pulse - chase labeling experiments in BHK - 21 cells demonstrate that the alpha ( 1B ) - AR is synthesized as a 70 kDa core Glycosylationglycosylated precursor that is converted to the 90 kDa mature form of the receptor with a half - time of approximately 2 h.
0.9939 Pulse - chase labeling experiments in BHK - 21 cells demonstrate that the Proteinalpha ( 1B ) - AR is synthesized as a 70 kDa core glycosylated precursor that is converted to the 90 kDa mature form of the receptor with a half - time of approximately 2 h.
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0.9754 N - Linked Glycosylationglycosylation of the alpha ( 1B ) - AR occurs at four asparagines on the N - terminus of the receptor.
0.9583 N - Linked glycosylation of the Proteinalpha ( 1B ) - AR occurs at four asparagines on the N - terminus of the receptor.
0.6148 N - Linked glycosylation of the alpha ( 1B ) - AR occurs at Entityfour asparagines on the N - terminus of the receptor.
0.8108 N - Linked glycosylation of the alpha ( 1B ) - AR occurs at four Entityasparagines on the N - terminus of the receptor.
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0.9890 Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the Proteinalpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.9365 Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.8950 Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.8607 Our findings demonstrate that N - linked glycosylation and Phosphorylationphosphorylation , but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.9494 Our findings demonstrate that N - linked Glycosylationglycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.9211 Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or O - linked Glycosylationglycosylation , contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.7408 Our findings demonstrate that GlycosylationN - linked glycosylation and phosphorylation, but not palmitoylation or O - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
0.6591 Our findings demonstrate that N - linked glycosylation and phosphorylation, but not palmitoylation or GlycosylationO - linked glycosylation, contribute to the structural heterogeneity of the alpha ( 1B ) - AR as it is observed in SDS - PAGE.
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0.9950 Our findings indicate that the Semliki Forest virus system can provide large amounts of functional and fully glycosylated Proteinalpha ( 1B ) - AR protein suitable for biochemical and structural studies.
0.9950 Our findings indicate that the Semliki Forest virus system can provide large amounts of functional and fully Glycosylationglycosylated alpha ( 1B ) - AR protein suitable for biochemical and structural studies.
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0.9960 Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic Proteinhistone deacetylase inhibitor inducing histone hyperacetylation, growth inhibition, and terminal cell differentiation.
0.9941 Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic histone deacetylase inhibitor inducing Proteinhistone hyperacetylation, growth inhibition, and terminal cell differentiation.
0.9219 Binding mode analysis of 3 - ( 4 - benzoyl - 1 - methyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamide : a new synthetic histone deacetylase inhibitor inducing histone Acetylationhyperacetylation , growth inhibition, and terminal cell differentiation.
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0.9816 The binding mode of 3 - ( 4 - aroyl - 1H - 2 - pyrrolyl ) - N - hydroxy - 2 - propenamides 1a - c, belonging to a recently reported class of synthetic Proteinhistone deacetylase ( HDAC ) inhibitors ( Massa, S. ; et al.
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0.9998 Chem. 2001, 44, 2069 - 2072 ), into the new modeled ProteinHDAC1 catalytic core is presented, and enzyme / inhibitor interactions are discussed.
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0.9996 ProteinHDAC1 X - ray coordinates were obtained by virtual " mutation " of those of histone deacetylase - like protein, a bacterial HDAC homologue.
0.9798 HDAC1 X - ray coordinates were obtained by virtual " mutation " of those of Proteinhistone deacetylase - like protein, a bacterial HDAC homologue.
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0.9995 In in vitro antimaize HD2 as well as antimouse ProteinHDAC1 assay, compounds 1a - c showed inhibitory activities in the low micromolar range.
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0.9962 Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased acetylation level of ProteinH4 as compared to control histones.
0.9948 Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced Proteinhistone hyperacetylation leading to a highly increased acetylation level of H4 as compared to control histones.
0.9940 Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased Acetylationacetylation level of H4 as compared to control histones.
0.9826 Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone Acetylationhyperacetylation leading to a highly increased acetylation level of H4 as compared to control histones.
0.9749 Similarly, 1a - c are endowed with anti - HDAC activity in vivo : on mouse A20 cells, 1a - c induced histone hyperacetylation leading to a highly increased acetylation level of H4 as compared to control Proteinhistones .
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0.9874 Hypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to factor inhibiting HIF Protein( FIH ) and is related to the cupin structural family.
0.8119 Hypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to Proteinfactor inhibiting HIF ( FIH ) and is related to the cupin structural family.
ProteinHypoxia - inducible factor ( HIF ) asparagine hydroxylase is identical to factor inhibiting HIF ( FIH ) and is related to the cupin structural family.
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0.9982 Hydroxylation of an asparagine residue in the C - terminal transactivation domain ( CAD ) of HIF - alpha abrogates interaction with Proteinp300 , preventing transcriptional activation.
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0.9891 Yeast two - hybrid assays recently identified factor inhibiting HIF Protein( FIH ) as a protein that associates with the CAD region of HIF - alpha.
0.8293 Yeast two - hybrid assays recently identified Proteinfactor inhibiting HIF ( FIH ) as a protein that associates with the CAD region of HIF - alpha.
0.5683 Yeast two - hybrid assays recently identified factor Proteininhibiting HIF ( FIH ) as a protein that associates with the CAD region of HIF - alpha.
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0.9997 Since FIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether ProteinFIH was the HIF asparaginyl hydroxylase.
0.9996 Since ProteinFIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether FIH was the HIF asparaginyl hydroxylase.
0.7733 Since FIH contains certain motifs present in iron - and 2 - OG - dependent oxygenases we investigated whether FIH was the ProteinHIF asparaginyl hydroxylase .
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0.9997 Assays using recombinant FIH and HIF - alpha fragments revealed that ProteinFIH is the enzyme that hydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen.
0.9995 Assays using recombinant ProteinFIH and HIF - alpha fragments revealed that FIH is the enzyme that hydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen.
0.8158 Assays using recombinant FIH and HIF - alpha fragments revealed that FIH is the enzyme that Hydroxylationhydroxylates the CAD asparagine residue, that the activity is directly inhibited by cobalt ( II ) and limited by hypoxia, and that the oxygen in the alcohol of the hydroxyasparagine residue is directly derived from dioxygen.
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0.9999 Sequence analyses involving ProteinFIH link the 2 - OG oxygenases with members of the cupin superfamily, including Zn ( II ) - utilizing phosphomannose isomerase, revealing structural and evolutionary links between these metal - binding proteins that share common motifs.
0.9628 Sequence analyses involving FIH link the 2 - OG oxygenases with members of the cupin superfamily, including Zn ( II ) - utilizing Proteinphosphomannose isomerase , revealing structural and evolutionary links between these metal - binding proteins that share common motifs.
0.7164 Sequence analyses involving FIH link the 2 - OG oxygenases with members of the cupin superfamily, including ProteinZn ( II ) - utilizing phosphomannose isomerase , revealing structural and evolutionary links between these metal - binding proteins that share common motifs.
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0.9993 ProteinFIH - 1 is an asparaginyl hydroxylase enzyme that regulates the transcriptional activity of hypoxia - inducible factor.
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0.8306 HIF transcriptional activity is suppressed under normoxic conditions by Hydroxylationhydroxylation of an asparagine residue within its C - terminal transactivation domain, blocking association with coactivators.
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0.9996 Here we show that the protein ProteinFIH - 1 , previously shown to interact with HIF, is an asparaginyl hydroxylase.
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0.9989 Like known hydroxylase enzymes, ProteinFIH - 1 is an Fe ( II ) - dependent enzyme that uses molecular O ( 2 ) to modify its substrate.
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0.9787 [ alpha ] - Secretase ADAM10 as well as Protein[ alpha ] APPs is reduced in platelets and CSF of Alzheimer disease patients.
0.9684 [ alpha ] - Secretase ProteinADAM10 as well as [ alpha ] APPs is reduced in platelets and CSF of Alzheimer disease patients.
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0.9161 BACKGROUND : Members of membrane - bound disintegrin metalloproteinases ( ADAMs ) were shown to be capable of cleaving amyloid precursor protein Protein( APP ) at the alpha - cleavage site in different cell systems.
0.8861 BACKGROUND : Members of membrane - bound disintegrin metalloproteinases ( ADAMs ) were shown to be capable of cleaving Proteinamyloid precursor protein ( APP ) at the alpha - cleavage site in different cell systems.
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0.9979 One of the candidate alpha - secretases identified in this family is ProteinADAM10 .
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0.9986 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ProteinADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.9234 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is Proteinperformed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.5594 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha ProteinAPPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.9990 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ProteinADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.9989 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ProteinADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.6958 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? ProteinMATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.6089 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.6018 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.5532 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ProteinADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
0.5130 The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 levels in the peripheral cells of AD patients related to a concomitant decrease in Proteinalpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
The present study addresses the following major questions : 1 ) Are the levels of an alpha - secretase candidate ( i. e., ADAM10 ) reduced in accessible cells of Alzheimer Disease ( AD ) patients? 2 ) Are ADAM10 Proteinlevels in the peripheral cells of AD patients related to a concomitant decrease in alpha APPs? MATERIALS AND METHODS : Western Blot analysis of ADAM10 is performed on platelet homogenates from 33 sporadic AD patients and on 26 age - matched control subjects.
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0.8160 Moreover, the levels of alpha - secretase metabolite Protein( alpha APPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody.
0.8325 Moreover, the levels of alpha - secretase metabolite ( alpha ProteinAPPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody.
0.5920 Moreover, the levels of alpha - secretase metabolite Protein( alpha APPs ) are tested both in platelets and cerebrospinal fluid ( CSF ) of the same pool of subjects by means of Western blot with a specific antibody.
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0.9984 RESULTS : A significant decrease of platelet ProteinADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of alpha APPs released from platelets.
0.9784 RESULTS : A significant decrease of platelet ADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of Proteinalpha APPs released from platelets.
0.5995 RESULTS : A significant decrease of platelet ADAM10 levels is observed in patients affected by probable AD when compared to control subjects and this is paralleled by a reduced level of alpha ProteinAPPs released from platelets.
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0.9375 Moreover, in the same pool of AD patients, Proteinalpha APPs levels were reduced concomitantly in CSF.
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0.9991 CONCLUSIONS : ProteinADAM10 is expressed in platelets.
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0.9993 A reduced level of ProteinADAM10 is observed in platelets obtained from AD patients compared to age - matched controls.
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0.9992 Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha APPs is present both in Proteinthrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells.
0.9955 Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of ProteinAPP processing might occur both in the neuronal compartment and peripheral cells.
0.9944 Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in Proteinalpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells.
0.9610 Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in alpha ProteinAPPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells.
0.5273 Further, in the same pool of AD patients, a qualitatively and quantitatively similar decrease in Proteinalpha APPs is present both in thrombin - activated platelets and CSF, thus suggesting that alterations of APP processing might occur both in the neuronal compartment and peripheral cells.
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0.9636 Reduced expression of the insulin - induced protein 1 and Proteinp41 Arp2 / 3 complex genes in human gastric cancers.
0.9342 Reduced expression of the Proteininsulin - induced protein 1 and p41 Arp2 / 3 complex genes in human gastric cancers.
Reduced expression of the insulin - induced protein 1 and p41 ProteinArp2 / 3 complex genes in human gastric cancers.
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0.9857 Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 ( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex Protein( p41 - Arc ) .
0.9848 Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 Protein( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex ( p41 - Arc ).
0.9452 Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : Insulin - induced protein 1 ( INSIG1 / CL - 6 ) and Proteinp41 Arp2 / 3 complex ( p41 - Arc ).
0.8389 Quantitative RT - PCR analysis of the 4 genes showed reduced expression of 2 genes in cancers : ProteinInsulin - induced protein 1 ( INSIG1 / CL - 6 ) and p41 Arp2 / 3 complex ( p41 - Arc ).
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0.9999 As for ProteinINSIG1 , a DNA fragment was derived from the edge of a CGI in the promoter region.
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0.9918 The edge was methylated in 11 of 22 primary gastric cancers, whereas the center was not DNA_methylationmethylated in any cancer.
0.9909 The edge was DNA_methylationmethylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer.
0.9346 The edge was methylated in 11 of 22 primary gastric cancers, whereas the Entitycenter was not methylated in any cancer.
0.9077 The Entityedge was methylated in 11 of 22 primary gastric cancers, whereas the center was not methylated in any cancer.
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0.9984 ProteinINSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the methylation.
0.9950 INSIG1 expression was markedly reduced in 19 cancers, including the 11 cancers with the DNA_methylationmethylation .
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0.9992 By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the methylation of the edge, partial restoration of ProteinINSIG1 expression was detected only in 2 of them.
0.9880 By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the methylation of the Entityedge , partial restoration of INSIG1 expression was detected only in 2 of them.
0.9879 By 5 - aza - 2'- deoxycytidine treatment of 5 cell lines with the DNA_methylationmethylation of the edge, partial restoration of INSIG1 expression was detected only in 2 of them.
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0.9971 These data indicated that, although the reduced ProteinINSIG1 expression in cancers was associated with the methylation at the edge of the CGI in the promoter region, the methylation was likely to be a secondary change.
0.9885 These data indicated that, although the reduced INSIG1 expression in cancers was associated with the DNA_methylationmethylation at the edge of the CGI in the promoter region, the methylation was likely to be a secondary change.
0.8987 These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the Entityedge of the CGI in the promoter region, the methylation was likely to be a secondary change.
0.9885 These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the CGI in the promoter region, the DNA_methylationmethylation was likely to be a secondary change.
0.9677 These data indicated that, although the reduced INSIG1 expression in cancers was associated with the methylation at the edge of the EntityCGI in the promoter region, the methylation was likely to be a secondary change.
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0.9988 As for Proteinp41 - Arc , a DNA fragment was derived from a CGI overlapping exon 8, and its methylation did not correlate with its expression.
0.9527 As for p41 - Arc, a DNA fragment was derived from a CGI overlapping exon 8, and its DNA_methylationmethylation did not correlate with its expression.
0.7971 As for p41 - Arc, a DNA fragment was derived from a EntityCGI overlapping exon 8 , and its methylation did not correlate with its expression.
0.8021 As for p41 - Arc, a DNA fragment was derived from a CGI overlapping Entityexon 8 , and its methylation did not correlate with its expression.
0.7886 As for p41 - Arc, a DNA fragment was derived from a CGI Entityoverlapping exon 8 , and its methylation did not correlate with its expression.
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0.9939 However, DNA_methylationmethylation of a CGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers.
0.9069 However, methylation of a EntityCGI in the promoter region with a marked reduction of its expression was observed in 1 of the 22 primary cancers.
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0.9999 INSIG1 and Proteinp41 - Arc are known to be involved in cellular differentiation and morphology, respectively, and it was suggested that their reduced expressions might be involved in gastric cancer development or progression.
0.9998 ProteinINSIG1 and p41 - Arc are known to be involved in cellular differentiation and morphology, respectively, and it was suggested that their reduced expressions might be involved in gastric cancer development or progression.
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0.9817 The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the hydroxylation of lysine in collagens I and ProteinII revealed by analysis of cross - linked telopeptides from urine.
0.9813 The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the Hydroxylationhydroxylation of lysine in collagens I and II revealed by analysis of cross - linked telopeptides from urine.
0.9658 The kyphoscoliotic type of Ehlers - Danlos syndrome ( type VI ) : differential effects on the hydroxylation of Entitylysine in collagens I and II revealed by analysis of cross - linked telopeptides from urine.
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0.9796 The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the lysyl hydroxylase 1 gene Protein( PLOD1 ) causing underhydroxylation of lysine residues in tissue collagens, particularly of skin.
0.7973 The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the Proteinlysyl hydroxylase 1 gene ( PLOD1 ) causing underhydroxylation of lysine residues in tissue collagens, particularly of skin.
0.5736 The kyphoscoliotic type of Ehlers - Danlos syndrome ( EDS type VIA ) ( OMIM 225400 ) is an autosomal recessive connective tissue disorder that results from mutations in the lysyl hydroxylase 1 gene ( PLOD1 ) causing underhydroxylation of Entitylysine residues in tissue collagens, particularly of skin.
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0.9998 Here we isolated cross - linked peptides containing these residues from the urine of a child with EDS VIA homozygous for a mutation that results in a stop codon and effective null expression of ProteinPLOD1 enzyme activity.
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0.8610 Peptides that had originated from bone type I collagen and cartilage Proteintype II collagen were identified.
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0.9621 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and Entity933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.9561 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been Hydroxylationhydroxylated .
0.9348 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of Proteinalpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.9304 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of Proteinalpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.8707 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at Entityresidues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.9294 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues Entity930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.8101 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical Entitylysines at residues 930 of alpha 1 ( I ) and 933 of alpha 2 ( I ) of the collagen triple - helix had not been hydroxylated.
0.6139 A cross - linked N - telopeptide fraction that is derived from bone type I collagen contained only LP, no HP, which means that the helical lysines at residues 930 of alpha 1 ( I ) and 933 of alpha Protein2 ( I ) of the collagen triple - helix had not been hydroxylated.
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0.9532 A second cross - linked peptide that is derived from the C - telopeptide domain of cartilage Proteintype II collagen showed both HP and LP in a 2 : 1 ratio, compared with 18 : 1 for the equivalent peptide from a normal child's urine.
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0.9299 The results show that in EDS VIA, bone type I collagen is more markedly underhydroxylated than cartilage Proteintype II collagen , at least at those helical sites that form cross - links.
0.2504 The results show that in EDS VIA, bone type I collagen is more markedly Glycosylationunderhydroxylated than cartilage type II collagen, at least at those helical sites that form cross - links.
The results show that in EDS VIA, bone type I collagen is more markedly Hydroxylationunderhydroxylated than cartilage type II collagen, at least at those helical sites that form cross - links.
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0.9989 Since ProteinPLOD1 is null, other PLOD genes must be responsible for the helical hydroxylation activity that results in HP.
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0.9348 The presented approach of analyzing urinary cross - linked C - telopeptide fragments of Proteintype II collagen may allow the detection of chondrodysplasias due to genetic defects in lysyl hydroxylase isoforms active in cartilage.
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0.9843 Postsynthetic Methylationtrimethylation of histone H4 at lysine 20 in mammalian tissues is associated with aging.
0.8944 Postsynthetic trimethylation of Proteinhistone H4 at lysine 20 in mammalian tissues is associated with aging.
0.8836 Postsynthetic trimethylation of histone H4 at Entitylysine 20 in mammalian tissues is associated with aging.
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0.9641 Methylation of the N - terminal region of Proteinhistones was first described more than 35 years ago, but its biological significance has remained unclear.
0.8936 Methylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear.
0.8667 MethylationMethylation of the N - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear.
0.8506 Methylation of the EntityN - terminal region of histones was first described more than 35 years ago, but its biological significance has remained unclear.
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0.9948 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and ProteinSuv39h1 , which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.9940 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases ProteinSUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.9753 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the ProteinH3 N terminus, this posttranslational modification has regained scientific interest.
0.9666 Primarily because of the recent discovery of the SET domain - depending ProteinH3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.9609 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.9606 Primarily because of the recent discovery of the SET domain - depending H3 - specific Proteinhistone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.5045 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Methylationmethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.9751 Primarily because of the recent discovery of the SET domain - depending ProteinH3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
0.7632 Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively methylate Entitylysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
Primarily because of the recent discovery of the SET domain - depending H3 - specific histone methyltransferases SUV39H1 and Suv39h1, which selectively Catalysismethylate lysine 9 of the H3 N terminus, this posttranslational modification has regained scientific interest.
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0.9890 In the past, investigations concerning the biological significance of histone Methylationmethylation were largely limited because of a lack of simple and sensitive analytical procedures for detecting this modification.
0.9868 In the past, investigations concerning the biological significance of Proteinhistone methylation were largely limited because of a lack of simple and sensitive analytical procedures for detecting this modification.
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0.9893 The present work investigated the Methylationmethylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and acetylated forms, which obviates the need to work with radioactive materials.
0.9753 The present work investigated the methylation pattern of Proteinhistone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and acetylated forms, which obviates the need to work with radioactive materials.
0.7084 The present work investigated the methylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of Methylationmethylated and acetylated forms, which obviates the need to work with radioactive materials.
0.7025 The present work investigated the methylation pattern of histone H4 both in different mammalian organs of various ages and in cell lines by applying mass spectrometric analysis and a newly developed hydrophilic - interaction liquid chromatographic method enabling the simultaneous separation of methylated and Acetylationacetylated forms, which obviates the need to work with radioactive materials.
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0.9705 In rat kidney and liver the Methylationdimethylated lysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts.
0.9286 In rat kidney and liver the dimethylated lysine 20 was found to be the main methylation product, whereas the Methylationmonomethyl derivative was present in much smaller amounts.
0.9131 In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts.
0.6436 In rat kidney and liver the dimethylated Entitylysine 20 was found to be the main methylation product, whereas the monomethyl derivative was present in much smaller amounts.
0.5199 In rat kidney and liver the dimethylated lysine 20 was found to be the main Methylationmethylation product, whereas the monomethyl derivative was present in much smaller amounts.
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0.9797 In addition, for the first time a Methylationtrimethylated form of lysine 20 of H4 was found in mammalian tissue.
0.9664 In addition, for the first time a trimethylated form of lysine 20 of ProteinH4 was found in mammalian tissue.
0.9549 In addition, for the first time a trimethylated form of Entitylysine 20 of H4 was found in mammalian tissue.
0.6508 In addition, for the first time a trimethylated form of Entitylysine 20 of H4 was found in mammalian tissue.
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0.9849 A significant increase in this Methylationtrimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ).
0.9770 A significant increase in this trimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and Methylationdimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ).
0.9747 A significant increase in this trimethylated histone H4 was detected in organs of animals older than 30 days, whereas the amounts of Methylationmono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ).
0.9511 A significant increase in this trimethylated Proteinhistone H4 was detected in organs of animals older than 30 days, whereas the amounts of mono - and dimethylated forms did not essentially change in organs from young ( 10 days old ) or old animals ( 30 and 450 days old ).
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0.9964 Trimethylated ProteinH4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated lysine 20 in cells in the stationary phase.
0.9951 Trimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in Methylationtrimethylated lysine 20 in cells in the stationary phase.
0.9903 MethylationTrimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated lysine 20 in cells in the stationary phase.
0.9192 Trimethylated H4 was also detected in transformed cells ; although it was present in only trace amounts in logarithmically growing cells, we found an increase in trimethylated Entitylysine 20 in cells in the stationary phase.
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0.9734 In the Proteincystathionine beta - synthase knockout mouse, elevations in total plasma homocysteine increase tissue S - adenosylhomocysteine, but responses of S - adenosylmethionine and DNA methylation are tissue specific.
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0.9700 The Proteincystathionine beta - synthase knockout mouse provides a unique opportunity to study biochemical consequences of a defective cystathionine beta - synthase enzyme.
0.9385 The cystathionine beta - synthase knockout mouse provides a unique opportunity to study biochemical consequences of a defective Proteincystathionine beta - synthase enzyme.
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0.9727 The present study was undertaken to assess the effect of elevated plasma total homocysteine caused by Proteincystathionine beta - synthase deficiency on one - carbon metabolism in 10 homozygous mutant mice and 10 age - and sex - matched wild - type mice.
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0.9716 The results of this study are consistent with the predicted role of Proteincystathionine beta - synthase in the regulation of plasma total homocysteine levels and tissue S - adenosylhomocysteine levels.
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0.9720 GlycosylationGlycosylation of human proteinase - activated receptor - 2 ( hPAR2 ) : role in cell surface expression and signalling.
0.9486 Glycosylation of human proteinase - activated receptor - 2 Protein( hPAR2 ) : role in cell surface expression and signalling.
0.6816 Glycosylation of human Proteinproteinase - activated receptor - 2 ( hPAR2 ) : role in cell surface expression and signalling.
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0.9764 We have analysed the role of N - linked glycosylation in regulating human proteinase - activated receptor - 2 Protein( hPAR ( 2 ) ) expression and function.
0.9109 We have analysed the role of GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function.
0.7643 We have analysed the role of N - linked glycosylation in regulating human Proteinproteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function.
0.9603 We have analysed the role of N - linked Glycosylationglycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function.
0.5297 We have analysed the role of GlycosylationN - linked glycosylation in regulating human proteinase - activated receptor - 2 ( hPAR ( 2 ) ) expression and function.
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0.9991 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or ProteinhPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9989 Epitope - tagged wild - type ProteinhPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9968 Epitope - tagged wild - type hPAR ( 2 ) Protein( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9940 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or ProteinhPAR ( 2 ) N30A , N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9907 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both Protein( hPAR ( 2 ) N30A , N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9727 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus Protein[ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9585 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or ProteinhPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.8938 Epitope - tagged wild - type hPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; ProteinhPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
0.9945 Epitope - tagged wild - type ProteinhPAR ( 2 ) ( wt - hPAR ( 2 ) ) or hPAR ( 2 ) that lacked glycosylation sequons ( following site - directed mutagenesis ) in either the N - terminus [ hPAR ( 2 ) N30A ( Asn ( 30 ) - - > Ala ) ], extracellular loop 2 [ ECL2 ; hPAR ( 2 ) N222Q ( Asn ( 222 ) - - > Gln ) or hPAR ( 2 ) N222A ( Asn ( 222 ) - - > Ala ) ] or both ( hPAR ( 2 ) N30A, N222A or hPAR ( 2 ) N30A, N222Q ) were expressed in the Chinese - hamster ovary ( CHO ) fibroblast cell line, Pro5.
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0.9982 Western blot analysis of Proteinwt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F deglycosylation.
0.9982 Western blot analysis of wt - hPAR ( 2 ) showed mature Proteinwt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F deglycosylation.
0.9305 Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following ProteinN - glycosidase F deglycosylation.
0.4976 Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Catalysisdeglycosylation .
0.9227 Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N Protein- glycosidase F deglycosylation.
Western blot analysis of wt - hPAR ( 2 ) showed mature wt - hPAR ( 2 ) to have a molecular mass of 55 - 100 kDa, and 33 - 48 kDa following N - glycosidase F Deglycosylationdeglycosylation .
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0.9998 FACS analysis and immunocytochemistry of the Proteinwt - hPAR ( 2 ) and PAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of wt - hPAR ( 2 ) ) cell surface expression.
0.9998 FACS analysis and immunocytochemistry of the wt - hPAR ( 2 ) and PAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of Proteinwt - hPAR ( 2 ) ) cell surface expression.
0.9998 FACS analysis and immunocytochemistry of the wt - hPAR ( 2 ) and ProteinPAR ( 2 ) mutant cell lines revealed that removal of both glycosylation sequons decreases ( 50 % of wt - hPAR ( 2 ) ) cell surface expression.
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0.9885 Western blot analysis indicated that both N - linked sites are Glycosylationglycosylated .
0.7699 Western blot analysis indicated that both EntityN - linked sites are glycosylated.
0.6745 Western blot analysis indicated that both EntityN - linked sites are glycosylated.
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0.9994 In functional studies, ProteinhPAR ( 2 ) N30A displayed a selective and significant increase in sensitivity towards tryptase.
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0.9993 Interestingly, hPAR ( 2 ) N222A displayed a loss in sensitivity towards all ProteinPAR ( 2 ) agonists tested.
0.9946 Interestingly, ProteinhPAR ( 2 ) N222A displayed a loss in sensitivity towards all PAR ( 2 ) agonists tested.
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0.9997 However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to ProteinPAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression.
0.9980 However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. ProteinhPAR ( 2 ) N30A , N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression.
0.9931 However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution ProteinhPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression.
0.9966 However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide ProteinSLIGRL - NH ( 2 ) , although this loss in sensitivity towards trypsin and SLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression.
0.9243 However, further analysis revealed receptor sensitivity to alanine mutations in this domain, as the more conservative substitution hPAR ( 2 ) N222Q displayed no change in response to PAR ( 2 ) agonists. hPAR ( 2 ) N30A, N222Q displayed increased sensitivity towards tryptase, but a loss in sensitivity towards trypsin and the synthetic peptide SLIGRL - NH ( 2 ), although this loss in sensitivity towards trypsin and ProteinSLIGRL - NH ( 2 ) was secondary to changes in cell - surface expression.
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0.9994 Finally, expression of sialic - acid - deficient Proteinwt - hPAR ( 2 ) in the CHO Lec2 glycosylation - deficient mutant cell line, showed a 40 kDa loss in molecular mass, in addition to a marked and selective increase in sensitivity towards tryptase.
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0.9991 We conclude that ProteinhPAR ( 2 ) N - linked glycosylation and sialylation regulates receptor expression and / or signalling.
0.8338 We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling.
0.8733 We conclude that hPAR ( 2 ) N - linked Glycosylationglycosylation and sialylation regulates receptor expression and / or signalling.
0.6257 We conclude that hPAR ( 2 ) GlycosylationN - linked glycosylation and sialylation regulates receptor expression and / or signalling.
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0.9201 ProteinN - acetyltransferase 2 genotype - related sulfapyridine acetylation and its adverse events.
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0.9802 Sulfapyridine ( SP ), one of the metabolites of sulfasalazine ( SASP ), is further metabolized into N - acetylsulfapyridine ( AcSP ) by polymorphic N - acetyltransferase 2 Protein( NAT2 ) .
0.8200 Sulfapyridine ( SP ), one of the metabolites of sulfasalazine ( SASP ), is further metabolized into N - acetylsulfapyridine ( AcSP ) by polymorphic ProteinN - acetyltransferase 2 ( NAT2 ).
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0.9994 ProteinNAT2 activity has been diagnosed by phenotyping, that is, evaluating plasma concentrations or urinary excretions of tentatively administered test drugs for dose individualization and avoidance of serious adverse events.
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0.9999 Herein, we investigated the relationship between ProteinNAT2 genotypes and the pharmacokinetics of SP in healthy Japanese subjects, as well as the adverse events of SASP in patients with inflammatory bowel disease ( IBD ).
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0.9997 Eight healthy subjects and 13 IBD patients were classified into three groups by ProteinNAT2 genotyping ; the homozygote for the wild - type allele ( Rapid Types ), the compound heterozygote for the wild - type and mutant alleles ( Intermediate Types ), and the homozygote for mutant alleles ( Slow Types ).
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0.9997 The ProteinNAT2 genotypes were well - correlated with the plasma concentrations or urinary excretions of SP and AcSP in 8 healthy subjects, except for one Slow Type.
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0.9997 In this case, the ProteinNAT2 activity was diagnosed by genotyping in advance, and the medical staff could pay scrupulous attention, resulting in no serious subjective symptoms such as abdominal pain, anorexia or fever.
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0.9999 Further investigations on the relationship between the ProteinNAT2 genotype and adverse events are required, although genotyping appeared to be a promising method to avoid such serious adverse events.
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0.9994 Histone H3 lysine 4 methylation is mediated by ProteinSet1 and promotes maintenance of active chromatin states in fission yeast.
0.9720 Histone H3 lysine 4 Methylationmethylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast.
0.8466 ProteinHistone H3 lysine 4 methylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast.
0.7979 Histone H3 Entitylysine 4 methylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast.
0.6807 Histone H3 lysine 4 methylation is Catalysismediated by Set1 and promotes maintenance of active chromatin states in fission yeast.
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0.9432 Methylation of Proteinhistone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.9095 MethylationMethylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.8615 Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 EntityLys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.8457 Methylation of histone H3 at Entitylysine 4 ( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.8383 Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or Entitylysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.7948 Methylation of histone H3 at lysine 4 ( H3 EntityLys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.6926 Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 Protein( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.6748 Methylation of histone H3 at lysine 4 Protein( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.5307 Methylation of histone H3 at lysine 4 ( H3 Lys - 4 ) or lysine 9 Entity( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
0.4543 Methylation of histone H3 at lysine 4 Entity( H3 Lys - 4 ) or lysine 9 ( H3 Lys - 9 ) is known to define active and silent chromosomal domains respectively from fission yeast to humans.
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0.9806 However, in budding yeast, H3 Lys - 4 Methylationmethylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA.
0.9711 However, in budding yeast, H3 EntityLys - 4 methylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA.
0.9638 However, in budding yeast, ProteinH3 Lys - 4 methylation is also necessary for silent chromatin assembly at telomeres and ribosomal DNA.
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0.9995 Here we demonstrate that deletion of Proteinset1 , which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 Lys - 4 methylation in fission yeast.
0.9882 Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes ProteinH3 Lys - 4 methylation in fission yeast.
0.9817 Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 EntityLys - 4 methylation in fission yeast.
0.9727 Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes H3 Lys - 4 Methylationmethylation in fission yeast.
0.5062 Here we demonstrate that deletion of set1, which encodes a protein containing an RNA recognition motif at its amino terminus and a SET domain at the carboxy terminus, abolishes EntityH3 Lys - 4 methylation in fission yeast.
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0.9135 Unlike in budding yeast, Set1 - mediated H3 Lys - 4 Methylationmethylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
0.6949 Unlike in budding yeast, CatalysisSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
0.6140 Unlike in budding yeast, Set1 - mediated ProteinH3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
0.5954 Unlike in budding yeast, Set1 - mediated H3 EntityLys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
0.4851 Unlike in budding yeast, ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
Unlike in budding yeast, ProteinSet1 - mediated H3 Lys - 4 methylation is not required for heterochromatin assembly at the silent mating - type region and centromeres in fission yeast.
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0.9939 Our analysis suggests that H3 Lys - 4 methylation is a stable Proteinhistone modification present throughout the cell cycle, including mitosis.
0.9929 Our analysis suggests that H3 Lys - 4 Methylationmethylation is a stable histone modification present throughout the cell cycle, including mitosis.
0.9775 Our analysis suggests that ProteinH3 Lys - 4 methylation is a stable histone modification present throughout the cell cycle, including mitosis.
0.9744 Our analysis suggests that H3 EntityLys - 4 methylation is a stable histone modification present throughout the cell cycle, including mitosis.
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0.9968 The loss of H3 Lys - 4 methylation in Proteinset1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9868 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 Acetylationacetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9852 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the ProteinH3 tail.
0.9817 The loss of H3 Lys - 4 Methylationmethylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9795 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 Methylationmethylation and acetylation of the H3 tail.
0.9785 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between ProteinH3 Lys - 4 methylation and acetylation of the H3 tail.
0.9783 The loss of ProteinH3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9774 The loss of H3 EntityLys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9662 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 EntityLys - 4 methylation and acetylation of the H3 tail.
0.9568 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in Proteinhistone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 tail.
0.9528 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and acetylation of the H3 Entitytail .
0.9435 The loss of H3 Lys - 4 methylation in set1Delta cells is correlated with a decrease in histone H3 acetylation levels, suggesting a mechanistic link between H3 Lys - 4 methylation and Acetylationacetylation of the H3 tail.
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0.9887 We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 Methylationmethylation .
0.9856 We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes ProteinH3 Lys - 9 methylation.
0.9843 We suggest that Methylationmethylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation.
0.9743 We suggest that methylation of ProteinH3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation.
0.9669 We suggest that methylation of H3 EntityLys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 Lys - 9 methylation.
0.9653 We suggest that methylation of H3 Lys - 4 primarily acts in the maintenance of transcriptionally poised euchromatic domains, and that this modification is dispensable for heterochromatin formation in fission yeast, which instead utilizes H3 EntityLys - 9 methylation.
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0.9643 Hypoxia - inducible factor asparaginyl hydroxylase Protein( FIH - 1 ) catalyses hydroxylation at the beta - carbon of asparagine - 803.
0.6652 ProteinHypoxia - inducible factor asparaginyl hydroxylase ( FIH - 1 ) catalyses hydroxylation at the beta - carbon of asparagine - 803.
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0.9913 Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the ProteinHIF - 1alpha / p300 interaction.
0.9737 EntityAsparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
0.9419 Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 Protein( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
0.8053 Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by Proteinfactor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
0.6968 Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Hydroxylationhydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
0.5802 Asparagine - 803 in the C - terminal transactivation domain of human Proteinhypoxia - inducible factor ( HIF ) - 1 alpha - subunit is hydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
Asparagine - 803 in the C - terminal transactivation domain of human hypoxia - inducible factor ( HIF ) - 1 alpha - subunit is Catalysishydroxylated by factor inhibiting HIF - 1 ( FIH - 1 ) under normoxic conditions causing abrogation of the HIF - 1alpha / p300 interaction.
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0.9586 NMR and other analyses of a hydroxylated HIF fragment produced in vitro demonstrate that hydroxylation occurs at the beta - carbon of EntityAsn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer.
0.9496 NMR and other analyses of a hydroxylated HIF fragment produced in vitro demonstrate that Hydroxylationhydroxylation occurs at the beta - carbon of Asn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer.
0.7227 NMR and other analyses of a Hydroxylationhydroxylated HIF fragment produced in vitro demonstrate that hydroxylation occurs at the beta - carbon of Asn - 803 and imply production of the threo - isomer, in contrast with other known aspartic acid / asparagine hydroxylases that produce the erythro - isomer.
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0.9986 The activity of serum GOT, ProteinGPT and alkaline phosphatase was also unchanged.
0.9984 The activity of serum ProteinGOT , GPT and alkaline phosphatase was also unchanged.
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0.9981 CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of caspase - 2 and Proteincaspase - 3 , cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in annexin V binding, and subsequent nuclear fragmentation.
0.9964 CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of Proteincaspase - 2 and caspase - 3, cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in annexin V binding, and subsequent nuclear fragmentation.
0.9861 CD437 and MM002 induce apoptosis in both cell lines, as indicated by the activation of caspase - 2 and caspase - 3, cleavage of poly ( adenosine diphosphate - ribose ) ( poly ( ADP - ribose ) ) polymerase, increase in Proteinannexin V binding, and subsequent nuclear fragmentation.
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0.9996 CD437 - mediated apoptosis was not associated with the modulation of ProteinBcl - 2 , Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form.
0.9994 CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or ProteinMcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form.
0.9993 CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, ProteinBax , or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form.
0.9830 CD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein ProteinBcl - X ( L ) to a proapoptotic 18 - kD form.
0.6090 ProteinCD437 - mediated apoptosis was not associated with the modulation of Bcl - 2, Bax, or Mcl - 1 levels, but was associated with the cleavage of the antiapoptotic protein Bcl - X ( L ) to a proapoptotic 18 - kD form.
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0.9979 This cleavage of ProteinBcl - X ( L ) was dependent on caspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk.
0.9970 This cleavage of Bcl - X ( L ) was dependent on Proteincaspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk.
0.9960 This cleavage of Bcl - X ( L ) was dependent on caspase - 3 activation since ProteinBcl - X ( L ) cleavage and apoptosis were inhibited by the caspase - 3 inhibitor Z - DVED - fmk.
0.9914 This cleavage of Bcl - X ( L ) was dependent on caspase - 3 activation since Bcl - X ( L ) cleavage and apoptosis were inhibited by the Proteincaspase - 3 inhibitor Z - DVED - fmk.
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0.9995 The product of the von Hippel - Lindau gene, ProteinpVHL , targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen.
0.5735 The product of the Proteinvon Hippel - Lindau gene , pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen.
0.8365 The product of the Proteinvon Hippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen.
0.6372 The product of the von ProteinHippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for polyubiquitination in the presence of oxygen.
0.6196 The product of the von Hippel - Lindau gene, pVHL, targets the alpha subunits of the heterodimeric transcription factor hypoxia - inducible factor ( HIF ) for Ubiquitinationpolyubiquitination in the presence of oxygen.
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0.9995 The binding of ProteinpVHL to HIF is governed by the enzymatic hydroxylation of conserved prolyl residues within peptidic motifs present in the HIFalpha family members.
0.6625 The binding of pVHL to HIF is governed by the enzymatic Hydroxylationhydroxylation of conserved prolyl residues within peptidic motifs present in the HIFalpha family members.
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0.9993 By using a biochemical purification strategy, we have identified a human homolog of Caenorhabditis elegans ProteinEgl9 as a HIF prolyl hydroxylase.
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0.8641 A model compound of this series stabilized HIF in a variety of cells, leading to the increased production of its downstream target, Proteinvascular endothelial growth factor .
0.5768 A model compound of this series stabilized HIF in a variety of cells, leading to the increased production of its downstream target, vascular Proteinendothelial growth factor .
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0.9573 Control of CBP co - activating activity by arginine Methylationmethylation .
0.9331 Control of ProteinCBP co - activating activity by arginine methylation.
0.9331 Control of CBP co - activating activity by Entityarginine methylation.
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0.9977 The histone acetyltransferases CREB binding protein ( CBP ) and the related Proteinp300 protein function as key transcriptional co - activators in multiple pathways.
0.9973 The Proteinhistone acetyltransferases CREB binding protein ( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways.
0.9768 The histone acetyltransferases CREB binding protein Protein( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways.
0.8809 The histone acetyltransferases ProteinCREB binding protein ( CBP ) and the related p300 protein function as key transcriptional co - activators in multiple pathways.
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0.9983 In the case of transcriptional activation by nuclear receptors, ligand promotes the recruitment of co - activators of the p160 family, such as ProteinGRIP - 1 .
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0.9997 AD1 binds CBP or p300, whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase ProteinCARM1 .
0.9996 AD1 binds CBP or Proteinp300 , whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase CARM1.
0.9992 AD1 binds ProteinCBP or p300, whereas AD2 has been shown to activate transcription through the recruitment of the arginine methyltransferase CARM1.
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0.9981 Recently, the KIX domain of CBP has been shown to be methylated by ProteinCARM1 in vitro.
0.9929 Recently, the KIX domain of ProteinCBP has been shown to be methylated by CARM1 in vitro.
0.7963 Recently, the EntityKIX domain of CBP has been shown to be methylated by CARM1 in vitro.
0.5521 Recently, the KIX domain of CBP has been shown to be Catalysismethylated by CARM1 in vitro.
0.5713 Recently, the EntityKIX domain of CBP has been shown to be methylated by CARM1 in vitro.
Recently, the KIX domain of CBP has been shown to be Methylationmethylated by CARM1 in vitro.
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0.9996 Here, we report that another domain of ProteinCBP is specifically methylated by CARM1 on conserved arginine residues in vitro and in vivo.
0.9994 Here, we report that another domain of CBP is specifically methylated by ProteinCARM1 on conserved arginine residues in vitro and in vivo.
0.5629 Here, we report that another domain of CBP is specifically Catalysismethylated by CARM1 on conserved arginine residues in vitro and in vivo.
Here, we report that another domain of CBP is specifically Methylationmethylated by CARM1 on conserved arginine residues in vitro and in vivo.
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0.9991 We also provide functional evidence that arginine residues methylated by ProteinCARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
0.9973 We also provide functional evidence that arginine residues methylated by CARM1 play a critical role in ProteinGRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
0.8416 We also provide functional evidence that Entityarginine residues methylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
0.4810 We also provide functional evidence that arginine residues Methylationmethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
0.7698 We also provide functional evidence that Entityarginine residues methylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
We also provide functional evidence that arginine residues Catalysismethylated by CARM1 play a critical role in GRIP - 1 - dependent transcriptional activation and in hormone - induced gene activation.
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0.9200 The hepatitis C virus ProteinRNA - dependent RNA polymerase membrane insertion sequence is a transmembrane segment.
0.6697 The hepatitis C virus RNA - dependent ProteinRNA polymerase membrane insertion sequence is a transmembrane segment.
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0.9795 The hepatitis C virus ( HCV ) RNA - dependent RNA polymerase Protein( RdRp ) belongs to a class of membrane proteins termed tail - anchored proteins.
0.8625 The hepatitis C virus ( HCV ) ProteinRNA - dependent RNA polymerase ( RdRp ) belongs to a class of membrane proteins termed tail - anchored proteins.
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0.9999 Here, we show that the HCV ProteinRdRp C - terminal membrane insertion sequence traverses the phospholipid bilayer as a transmembrane segment.
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0.9998 Moreover, the HCV ProteinRdRp was found to be retained in the endoplasmic reticulum ( ER ) or an ER - derived modified compartment both following transient transfection and in the context of a subgenomic replicon.
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0.9678 Molecular and biochemical characterisation of a novel sulphatase gene : Arylsulfatase G Protein( ARSG ) .
0.8697 Molecular and biochemical characterisation of a novel sulphatase gene : ProteinArylsulfatase G ( ARSG ).
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0.9786 Through bioinformatic searches of the EST database, we have identified a novel gene consisting of 11 exons and encoding a 525 aa protein that shares a high degree of sequence similarity with all sulphatases and in particular with arylsulphatases, hence the tentative name Arylsulfatase G Protein( ARSG ) .
0.9090 Through bioinformatic searches of the EST database, we have identified a novel gene consisting of 11 exons and encoding a 525 aa protein that shares a high degree of sequence similarity with all sulphatases and in particular with arylsulphatases, hence the tentative name ProteinArylsulfatase G ( ARSG ).
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0.9628 The highest homology is shared with ProteinArylsulfatase A , a lysosomal sulphatase which is mutated in metachromatic leukodistrophy, particularly in the amino - terminal region.
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0.9778 The murine homologue of ProteinArylsulfatase G gene product shows 87 % identity with the human protein.
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0.9556 To test the function of this novel gene we transfected the full - length cDNA in Cos7 cells, and detected an ProteinArylsulfatase G precursor protein of 62 kDa.
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0.9557 After Glycosylationglycosylation the precursor is maturated in a 70 kDa form, which localises to the endoplasmic reticulum.
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0.9614 Northern blot analysis of ProteinArylsulfatase G revealed a ubiquitous expression pattern.
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0.9161 Further studies are needed to characterise the function of ProteinArylsulfatase G , possibly revealing a novel metabolic pathway.
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0.9915 Gene - specific targeting of H3K9 Methylationmethylation is sufficient for initiating repression in vivo.
0.4964 Gene - specific targeting of EntityH3K9 methylation is sufficient for initiating repression in vivo.
Gene - specific targeting of ProteinH3K9 methylation is sufficient for initiating repression in vivo.
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0.9796 Histone H3 lysine 9 ( H3K9 ) Methylationmethylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms.
0.8773 Histone H3 Entitylysine 9 ( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms.
0.8742 ProteinHistone H3 lysine 9 ( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms.
0.6420 Histone H3 lysine 9 Protein( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms.
Histone H3 lysine 9 Entity( H3K9 ) methylation is an epigenetic signal that is recognized by HP1 and correlates with gene silencing in a variety of organisms.
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0.9932 Discovery of the enzymes that catalyze H3K9 Methylationmethylation has identified a second gene - specific function for this modification in transcriptional repression.
0.5202 Discovery of the enzymes that catalyze EntityH3K9 methylation has identified a second gene - specific function for this modification in transcriptional repression.
Discovery of the enzymes that catalyze ProteinH3K9 methylation has identified a second gene - specific function for this modification in transcriptional repression.
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0.9751 Whether H3K9 Methylationmethylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown.
0.6680 Whether EntityH3K9 methylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown.
Whether ProteinH3K9 methylation is causative in the initiation and establishment of gene repression or is a byproduct of the process leading to the repressed state remains unknown.
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0.9816 To investigate the role of HMTs and specifically H3K9 Methylationmethylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene.
0.6073 To investigate the role of HMTs and specifically EntityH3K9 methylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene.
To investigate the role of HMTs and specifically ProteinH3K9 methylation in gene repression, we have employed engineered zinc - finger transcription factors ( ZFPs ) to target HMT activity to a specific endogenous gene.
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0.9995 By utilizing ZFPs that recognize the promoter of the endogenous ProteinVEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone H3K9 and the consequent repression of target gene expression.
0.9609 By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local Methylationmethylation of histone H3K9 and the consequent repression of target gene expression.
0.9582 By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone EntityH3K9 and the consequent repression of target gene expression.
0.5971 By utilizing ZFPs that recognize the promoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of Proteinhistone H3K9 and the consequent repression of target gene expression.
0.5517 By utilizing ZFPs that recognize the Entitypromoter of the endogenous VEGF - A gene, and thus employing this chromosomal locus as an in vivo reporter, we show that ZFPs linked to a minimal catalytic HMT domain affect local methylation of histone H3K9 and the consequent repression of target gene expression.
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0.9805 Thus, H3K9 Methylationmethylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo.
0.6792 Thus, EntityH3K9 methylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo.
Thus, ProteinH3K9 methylation is a primary signal that is sufficient for initiating a gene repression pathway in vivo.
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0.9998 The majority of the SeCys conjugates produced near complete inhibition of ProteinCYP1A1 at a concentration of 250 microm.
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0.9988 CYP2C9, Protein- 2C19 and - 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates.
0.9982 CYP2C9, - 2C19 and Protein- 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates.
0.9980 ProteinCYP2C9 , - 2C19 and - 2D6 were moderately ( 50 - 60 % ) inhibited by the SeCys conjugates.
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0.9986 CYP1A2, Protein- 2E1 and - 3A4 were least inhibited. 3.
0.9985 ProteinCYP1A2 , - 2E1 and - 3A4 were least inhibited. 3.
0.9975 CYP1A2, - 2E1 and Protein- 3A4 were least inhibited. 3.
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0.9998 Studies on the susceptibility of ProteinCYP1A1 to SeCys conjugates implicated a thiol - reactive intermediate, as evidenced by reduced inhibition levels in the presence of glutathione and N - acetyl cysteine.
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0.9974 N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, - 2C19, - 2E1 and Protein- 3A4 .
0.9970 N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, - 2C19, Protein- 2E1 and - 3A4.
0.9967 N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards ProteinCYP1A2 , - 2C19, - 2E1 and - 3A4.
0.9956 N - acetylation of SeCys conjugates consistently increased the inhibitory potency towards CYP1A2, Protein- 2C19 , - 2E1 and - 3A4.
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0.9997 It is concluded that the potent and relatively selective ProteinCYP1A1 inhibition exerted by SeCys conjugates may contribute to their chemopreventive activity.
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0.9988 Identification of a lactoferrin - derived peptide possessing binding activity to hepatitis C virus ProteinE2 envelope protein.
0.9945 Identification of a Proteinlactoferrin - derived peptide possessing binding activity to hepatitis C virus E2 envelope protein.
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0.9995 Bovine and human lactoferrins ( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between ProteinLF and HCV.
0.9830 Bovine and human lactoferrins Protein( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between LF and HCV.
0.9812 Bovine and human Proteinlactoferrins ( LF ) prevent hepatitis C virus ( HCV ) infection in cultured human hepatocytes ; the preventive mechanism is thought to be the direct interaction between LF and HCV.
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0.9979 To clarify this hypothesis, we have characterized the binding activity of LF to HCV ProteinE2 envelope protein and have endeavored to determine which region ( s ) of LF are important for this binding activity.
0.9955 To clarify this hypothesis, we have characterized the binding activity of ProteinLF to HCV E2 envelope protein and have endeavored to determine which region ( s ) of LF are important for this binding activity.
0.9952 To clarify this hypothesis, we have characterized the binding activity of LF to HCV E2 envelope protein and have endeavored to determine which region ( s ) of ProteinLF are important for this binding activity.
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0.9994 Several regions of human ProteinLF have been expressed and purified as thioredoxin - fused proteins in Escherichia coli.
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0.9996 Far - Western blot analysis using these LF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of ProteinLF specifically bound to the E2 protein.
0.9995 Far - Western blot analysis using these LF fragments and the ProteinE2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the E2 protein.
0.9993 Far - Western blot analysis using these LF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the ProteinE2 protein.
0.9976 Far - Western blot analysis using these ProteinLF fragments and the E2 protein, expressed in Chinese hamster ovary cells, revealed that the 93 carboxyl amino acids of LF specifically bound to the E2 protein.
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0.9996 The 93 carboxyl amino acids of ProteinLFs derived from bovine and horse cells also possessed similar binding activity to the E2 protein.
0.9995 The 93 carboxyl amino acids of LFs derived from bovine and horse cells also possessed similar binding activity to the ProteinE2 protein.
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0.9996 In addition, the amino acid sequences of these carboxyl regions appeared to show partial homology to ProteinCD81 , a candidate receptor for HCV, and the binding activity of these carboxyl regions was also comparable with that of CD81.
0.9993 In addition, the amino acid sequences of these carboxyl regions appeared to show partial homology to CD81, a candidate receptor for HCV, and the binding activity of these carboxyl regions was also comparable with that of ProteinCD81 .
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0.9982 Further deletion analysis identified 33 amino acid residues as the minimum binding site in the carboxyl region of ProteinLF , and the binding specificity of these 33 amino acids was also confirmed by using 33 maltose - binding protein - fused amino acids.
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0.9200 Furthermore, we demonstrated that the 33 Proteinmaltose - binding protein - fused amino acids prevented HCV infection in cultured human hepatocytes.
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0.9994 In addition, the site - directed mutagenesis to an Ala residue in both terminal residues of the 33 amino acids revealed that Cys at amino acid 628 was determined to be critical for binding to the ProteinE2 protein.
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0.9992 This is the first identification of a natural protein - derived peptide that specifically binds to HCV ProteinE2 protein and prevents HCV infection.
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0.9970 Glucocorticoid suppression of nuclear factor - kappa B : a role for Proteinhistone modifications.
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0.9980 These bind to, and activate, co - activator molecules that then acetylate core Proteinhistones resulting in elevated gene transcription.
0.9838 These bind to, and activate, co - activator molecules that then Acetylationacetylate core histones resulting in elevated gene transcription.
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0.9993 Corticosteroids reverse histone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of Proteinhistone deacetylases to the activated transcription complex.
0.9971 Corticosteroids reverse Proteinhistone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex.
0.9951 Corticosteroids reverse histone Acetylationacetylation at the site of inflammatory gene transcription, either by direct binding of the activated glucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex.
0.9606 Corticosteroids reverse histone acetylation at the site of inflammatory gene transcription, either by direct binding of the activated Proteinglucocorticoid receptor to NF - kappa B - associated co - activators or by recruitment of histone deacetylases to the activated transcription complex.
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0.9929 Probing the conformational and dynamical effects of O - glycosylation within the immunodominant region of a ProteinMUC1 peptide tumor antigen.
0.9927 Probing the conformational and dynamical effects of GlycosylationO - glycosylation within the immunodominant region of a MUC1 peptide tumor antigen.
0.7962 Probing the conformational and dynamical effects of O - glycosylation within the Entityimmunodominant region of a MUC1 peptide tumor antigen.
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0.9826 ProteinMUC1 mucin is a large transmembrane glycoprotein, the extracellular domain of which is formed by a repeating 20 amino acid sequence, GVTSAPDTRPAPGSTAPPAH.
0.5706 MUC1 mucin is a large transmembrane glycoprotein, the extracellular domain of which is formed by a repeating 20 amino acid sequence, ProteinGVTSAPDTRPAPGSTAPPAH .
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0.9895 However, in neoplastic breast tissue, the extracellular domain is Glycosylationunder - glycosylated , resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9833 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core EntityTn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9695 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9624 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9619 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn Entity( GalNAc ) , STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.8804 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates.
0.8337 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn Entity( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9785 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 EntityGalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9575 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 EntityGalNAc ) carbohydrates.
0.9523 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core EntityTn ( GalNAc ) , STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9232 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl Entityalpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.9076 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal Entitybeta1 - 3 GalNAc ) carbohydrates.
0.8761 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.8266 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.7873 However, in neoplastic breast tissue, the extracellular Entitydomain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.7721 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl Entityalpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.7588 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.7582 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal Entitybeta1 - 3 GalNAc ) carbohydrates.
0.7263 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates.
0.7236 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and EntityTF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.6652 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.6415 However, in neoplastic breast tissue, the Glycosylationextracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.6345 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF Entity( Gal beta1 - 3 GalNAc ) carbohydrates.
0.6316 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn Entity( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.6209 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), EntitySTn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
0.5170 However, in neoplastic breast tissue, the extracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 EntityGalNAc ) carbohydrates .
However, in neoplastic breast tissue, the Entityextracellular domain is under - glycosylated, resulting in the exposure of a highly immunogenic core peptide epitope ( PDTRP in bold above ), as well as in the exposure of normally cryptic core Tn ( GalNAc ), STn ( sialyl alpha2 - 6 GalNAc ) and TF ( Gal beta1 - 3 GalNAc ) carbohydrates.
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0.6019 Here, we report the results of 1H NMR structural studies, natural abundance 13C NMR relaxation measurements and distance - restrained MD simulations designed to probe the structural and dynamical effects of GlycosylationTn - glycosylation within the PDTRP core peptide epitope.
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0.9968 Two synthetic peptides were studied : a nine - residue ProteinMUC1 peptide of the sequence, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9, and a Tn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9.
0.9156 Two synthetic peptides were studied : a nine - residue MUC1 peptide of the sequence, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9, and a GlycosylationTn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9.
0.6593 Two synthetic peptides were studied : a nine - residue MUC1 peptide of the sequence, EntityThr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 - Arg7 - Pro8 - Ala9 , and a Tn - glycosylated version of this peptide, Thr1 - Ser2 - Ala3 - Pro4 - Asp5 - Thr6 ( alphaGalNAc ) - Arg7 - Pro8 - Ala9.
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0.9973 The results of these studies show that a type I beta - turn conformation is adopted by residues PDTR within the PDTRP region of the unglycosylated ProteinMUC1 sequence.
0.9303 The results of these studies show that a type I beta - turn conformation is adopted by residues PDTR within the PDTRP region of the Glycosylationunglycosylated MUC1 sequence.
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0.9935 The existence of a similar beta - turn within the PDTRP core peptide epitope of the Glycosylationunder - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems.
0.9255 The existence of a similar beta - turn within the PDTRP core peptide epitope of the under - glycosylated cancer - associated ProteinMUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems.
0.7533 The existence of a similar beta - turn within the PDTRP core peptide Entityepitope of the under - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems.
The existence of a similar beta - turn within the EntityPDTRP core peptide epitope of the under - glycosylated cancer - associated MUC1 mucin protein might explain the immunodominance of this region in vivo, as the presence of defined secondary structure within peptide epitope regions has been correlated with increased immunogenicity in other systems.
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0.8089 Our results have also shown that Tn Glycosylationglycosylation at the central threonine within the PDTRP core epitope region shifts the conformational equilibrium away from the type I beta - turn conformation and toward a more rigid and extended state.
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0.9996 The significance of these results are discussed in relation to the possible roles that peptide epitope secondary structure and glycosylation state may play in ProteinMUC1 tumor immunogenicity.
0.9714 The significance of these results are discussed in relation to the possible roles that peptide epitope secondary structure and Glycosylationglycosylation state may play in MUC1 tumor immunogenicity.
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0.9743 EntityLysine - 79 of histone H3 is hypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation.
0.9735 Lysine - 79 of histone H3 is Methylationhypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation.
0.9558 Lysine - 79 of Proteinhistone H3 is hypomethylated at silenced loci in yeast and mammalian cells : a potential mechanism for position - effect variegation.
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0.9465 Methylation of lysine - 79 ( K79 ) within the globular domain of Proteinhistone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
0.9322 Methylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by ProteinDot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
0.9133 Methylation of lysine - 79 Entity( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
0.8890 Methylation of Entitylysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
0.7087 MethylationMethylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
CatalysisMethylation of lysine - 79 ( K79 ) within the globular domain of histone H3 by Dot1 methylase is important for transcriptional silencing and for association of the Sir silencing proteins in yeast.
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0.9696 Here, we show that the level of H3 - K79 Methylationmethylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions.
0.4977 Here, we show that the level of EntityH3 - K79 methylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions.
Here, we show that the level of ProteinH3 - K79 methylation is low at all Sir - dependent silenced loci but not at other transcriptionally repressed regions.
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0.8828 MethylationHypomethylation of H3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins.
0.5668 Hypomethylation of ProteinH3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins.
Hypomethylation of EntityH3 - K79 at the telomeric and silent mating - type loci, but not the ribosomal DNA, requires the Sir proteins.
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0.9980 Overexpression of ProteinSir3 concomitantly extends the domain of Sir protein association and H3 - K79 hypomethylation at telomeres.
0.9036 Overexpression of Sir3 concomitantly extends the domain of Sir protein association and H3 - K79 Methylationhypomethylation at telomeres.
0.6012 Overexpression of Sir3 concomitantly extends the domain of Sir protein association and EntityH3 - K79 hypomethylation at telomeres.
Overexpression of Sir3 concomitantly extends the domain of Sir protein association and ProteinH3 - K79 hypomethylation at telomeres.
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0.9888 In mammalian cells, H3 - K79 Methylationmethylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic.
0.5263 In mammalian cells, EntityH3 - K79 methylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic.
In mammalian cells, ProteinH3 - K79 methylation is found at loci that are active for V ( D ) J recombination, but not at recombinationally inactive loci that are heterochromatic.
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0.9973 These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of ProteinDot1 to methylate histone H3.
0.9796 These results suggest that H3 - K79 Methylationmethylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3.
0.9361 These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate Proteinhistone H3 .
0.9027 These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to Methylationmethylate histone H3.
0.5730 These results suggest that ProteinH3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3.
These results suggest that EntityH3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to methylate histone H3.
These results suggest that H3 - K79 methylation is an evolutionarily conserved marker of active chromatin regions, and that silencing proteins block the ability of Dot1 to Catalysismethylate histone H3.
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0.9930 Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block H3 - K79 Methylationmethylation .
0.9891 Further, they suggest that Sir proteins preferentially bind chromatin with Methylationhypomethylated H3 - K79 and then block H3 - K79 methylation.
0.5344 Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated EntityH3 - K79 and then block H3 - K79 methylation.
0.5262 Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block EntityH3 - K79 methylation.
Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated ProteinH3 - K79 and then block H3 - K79 methylation.
Further, they suggest that Sir proteins preferentially bind chromatin with hypomethylated H3 - K79 and then block ProteinH3 - K79 methylation.
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0.9815 This positive feedback loop, and the reverse loop in which H3 - K79 Methylationmethylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation.
0.4951 This positive feedback loop, and the reverse loop in which ProteinH3 - K79 methylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation.
This positive feedback loop, and the reverse loop in which EntityH3 - K79 methylation weakens Sir protein association and leads to further methylation, suggests a model for position - effect variegation.
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0.9717 Cyclosporin A prevents the hypoxic adaptation by activating hypoxia - inducible factor - 1alpha EntityPro - 564 hydroxylation.
0.9477 Cyclosporin A prevents the hypoxic adaptation by activating hypoxia - inducible factor - 1alpha Pro - 564 Hydroxylationhydroxylation .
0.6583 Cyclosporin A prevents the hypoxic adaptation by activating Proteinhypoxia - inducible factor - 1alpha Pro - 564 hydroxylation.
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0.9987 The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of ProteinHIF - 1alpha to the ubiquitin - proteasome pathway.
0.9985 The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the Proteinubiquitin - proteasome pathway.
0.9351 The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau Protein( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway.
0.6907 The mechanism by which hypoxia induces gene transcription involves the inhibition of hypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents Proteinvon Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway.
0.5809 The mechanism by which hypoxia induces gene transcription involves the inhibition of Proteinhypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway.
The mechanism by which hypoxia induces gene transcription involves the inhibition of Proteinhypoxia - inducible factor ( HIF ) - 1alpha prolyl hydroxylase activity, which prevents von Hippel - Lindau ( vHL ) - dependent targeting of HIF - 1alpha to the ubiquitin - proteasome pathway.
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0.9991 ProteinHIF - 1alpha is stabilized, translocates to the nucleus, interacts with hypoxia - responsive elements, and promotes the activation of target genes.
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0.9979 CsA inhibits hypoxia - dependent gene transcription in a reporter gene assay and prevents the hypoxic accumulation of ProteinHIF - 1alpha .
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0.9992 Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of ProteinHIF - 1alpha to the green fluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner.
0.9878 Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the green fluorescent protein Protein( GFP ) destabilized the protein in an oxygen - dependent manner.
0.9178 Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the Proteingreen fluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner.
0.6449 Addition of the 530 - 603 C - terminal oxygen - dependent degradation ( ODD ) domain of HIF - 1alpha to the green Proteinfluorescent protein ( GFP ) destabilized the protein in an oxygen - dependent manner.
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0.9812 CsA prevented the hypoxic stabilization of an ODD Protein. GFP fusion protein.
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0.9990 CsA stimulated the enzymatic activity in the presence of a peptide that mimicked the 557 - 576 sequence of ProteinHIF - 1alpha .
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0.9857 The enzyme promoted Protein[ ( 35 ) S ] vHL binding to glutathione S - transferase ( GST ). ODD fusion protein.
0.6056 The enzyme promoted [ ( 35 ) S ] vHL binding to Proteinglutathione S - transferase ( GST ). ODD fusion protein.
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0.9991 CsA effects were not observed when the proline residue corresponding to Pro - 564 in the ProteinHIF - 1alpha sequence was replaced by a hydroxyproline or an alanine residue.
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0.9988 Finally, CsA increased ProteinvHL - ODD interaction during hypoxia.
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0.9986 We conclude that CsA destabilizes ProteinHIF - 1alpha by promoting hydroxylation of Pro - 564 in the ODD domain.
0.9597 We conclude that CsA destabilizes HIF - 1alpha by promoting Hydroxylationhydroxylation of Pro - 564 in the ODD domain.
0.9593 We conclude that CsA destabilizes HIF - 1alpha by promoting hydroxylation of EntityPro - 564 in the ODD domain.
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0.9995 A gene encoding a yeast peptide : N - glycanase, ProteinPNG1 , has been cloned, but this N - glycanase and its mammalian homolog were reported to be incapable of deglycosylating full - length glycoproteins.
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0.9996 We show that both the yeast ProteinPNG1 enzyme and its mammalian homolog display N - glycanase activity towards intact glycoproteins.
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0.9987 As substrates, cytosolic ProteinPNGase activity prefers proteins containing high - mannose over those bearing complex type oligosaccharides.
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0.9999 Importantly, ProteinPNG1 discriminates between non - native and folded glycoproteins, consistent with a role for N - glycanase in cytoplasmic turnover of glycoproteins.
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0.9984 Preclinical evaluation of antineoplastic activity of inhibitors of DNA methylation ( 5 - aza - 2'- deoxycytidine ) and Proteinhistone deacetylation ( trichostatin A, depsipeptide ) in combination against myeloid leukemic cells.
0.8599 Preclinical evaluation of antineoplastic activity of inhibitors of DNA methylation ( 5 - aza - 2'- deoxycytidine ) and histone Deacetylationdeacetylation ( trichostatin A, depsipeptide ) in combination against myeloid leukemic cells.
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0.9967 During the development of leukemia, genes that suppress growth and induce differentiation can be silenced by aberrant DNA methylation and by changes in chromatin structure that involve Proteinhistone deacetylation.
0.9130 During the development of leukemia, genes that suppress growth and induce differentiation can be silenced by aberrant DNA methylation and by changes in chromatin structure that involve histone Deacetylationdeacetylation .
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0.9962 It has been reported that a positive interaction between DNA methylation and Proteinhistone deacetylation takes place to inhibit transcription.
0.8901 It has been reported that a positive interaction between DNA methylation and histone Deacetylationdeacetylation takes place to inhibit transcription.
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0.9993 ProteinHistone deacetylase inhibitors ( HDI ) can also activate gene expression in leukemic cell lines by producing changes in chromatin configuration, and show antineoplastic activity in preclinical studies.
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0.9931 Complex - type biantennary N - glycans of recombinant human Proteintransferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and [ beta ] - 1, 2 - N - acetylglucosaminyltransferase II.
0.5402 Complex - type biantennary N - glycans of recombinant human transferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and Protein[ beta ] - 1, 2 - N - acetylglucosaminyltransferase II .
0.6196 Complex - type biantennary N - glycans of recombinant human transferrin from Trichoplusia ni insect cells expressing mammalian [ beta ] - 1, 4 - galactosyltransferase and [ beta ] - 1 Protein, 2 - N - acetylglucosaminyltransferase II .
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0.9994 A novel recombinant baculovirus expression vector was used to produce His - tagged human Proteintransferrin in a transformed insect cell line ( Tn5beta4GalT ) that constitutively expresses a mammalian beta - 1, 4 - galactosyltransferase.
0.7021 A novel recombinant baculovirus expression vector was used to produce His - tagged human transferrin in a transformed insect cell line Protein( Tn5beta4GalT ) that constitutively expresses a mammalian beta - 1, 4 - galactosyltransferase.
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0.9981 This virus encoded the His - tagged human Proteintransferrin protein in conventional fashion under the control of the very late polyhedrin promoter.
0.9892 This virus encoded the His - tagged human transferrin protein in conventional fashion under the control of the very late Proteinpolyhedrin promoter.
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0.9649 In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early Protein( ie1 ) promoter.
0.5298 In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human Proteinbeta - 1, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter.
0.6877 In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1, 2 - ProteinN - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter.
0.5578 In addition, to enhance the synthesis of galactosylated biantennary N - glycans, this virus encoded human beta - 1 Protein, 2 - N - acetylglucosaminyltransferase II under the control of an immediate - early ( ie1 ) promoter.
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0.9988 Detailed analyses by MALDI - TOF MS, exoglycosidase digestion, and two - dimensional HPLC revealed that the N - glycans on the purified recombinant human Proteintransferrin produced by this virus - host system included four different fully galactosylated, biantennary, complex - type glycans.
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0.9169 Overexpression of the ProteinCT GalNAc transferase inhibits muscular dystrophy in a cleavage - resistant dystroglycan mutant mouse.
0.5200 Overexpression of the CT ProteinGalNAc transferase inhibits muscular dystrophy in a cleavage - resistant dystroglycan mutant mouse.
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0.9982 Transgenic mice that express Proteindystroglycan containing a serine to alanine point mutation at the normal site of cleavage ( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved dystroglycan and have muscular dystrophy [ Neuromusc.
0.9977 Transgenic mice that express dystroglycan containing a serine to alanine point mutation at the normal site of cleavage ( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved Proteindystroglycan and have muscular dystrophy [ Neuromusc.
0.9892 Transgenic mice that express dystroglycan containing a serine to alanine point mutation at the normal site of cleavage Protein( DG ( S654A ) ) in their skeletal muscles fail to express endogenously cleaved dystroglycan and have muscular dystrophy [ Neuromusc.
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0.9897 Dystrophic ProteinDG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on alpha dystroglycan, a finding similar to muscles in some forms of congenital muscular dystrophy.
0.8732 Dystrophic DG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on Proteinalpha dystroglycan , a finding similar to muscles in some forms of congenital muscular dystrophy.
0.7869 Dystrophic DG ( S654A ) muscles have reduced binding of antibodies, including VIA4 - 1, that recognize carbohydrate antigens on alpha Proteindystroglycan , a finding similar to muscles in some forms of congenital muscular dystrophy.
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0.9952 Here we describe one ProteinDG ( S654A ) transgenic line where VIA4 - 1 antibody binding is absent in skeletal muscle.
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0.8865 One such modification is likely to be the CT carbohydrate antigen, which is present on alpha dystroglycan in muscles overexpressing the ProteinCT GalNAc transferase [ Dev.
0.5733 One such modification is likely to be the CT carbohydrate antigen, which is present on alpha dystroglycan in muscles overexpressing the CT ProteinGalNAc transferase [ Dev.
0.5548 One such modification is likely to be the CT carbohydrate antigen, which is present on Proteinalpha dystroglycan in muscles overexpressing the CT GalNAc transferase [ Dev.
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0.9634 To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made DG ( S654A ) / CT GalNAc transferase Protein( DG ( S654A ) / CT ) transgenic mice.
0.9532 To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made ProteinDG ( S654A ) / CT GalNAc transferase ( DG ( S654A ) / CT ) transgenic mice.
0.5933 To test the relationship between the VIA4 - 1 and CT carbohydrate antigens, we made ProteinDG ( S654A ) / CT GalNAc transferase ( DG ( S654A ) / CT ) transgenic mice.
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0.9874 Surprisingly, dystroglycan was cleaved, and alpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in ProteinDG ( S654A ) / CT muscles.
0.9872 Surprisingly, Proteindystroglycan was cleaved, and alpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles.
0.9840 Surprisingly, dystroglycan was cleaved, and alpha dystroglycan was Glycosylationglycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles.
0.7953 Surprisingly, dystroglycan was cleaved, and Proteinalpha dystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles.
0.7708 Surprisingly, dystroglycan was cleaved, and alpha Proteindystroglycan was glycosylated with the VIA4 - 1 antigen, in DG ( S654A ) / CT muscles.
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0.9986 In addition, muscles in ProteinDG ( S654A ) / CT transgenic mice had little or no evidence of muscular dystrophy when compared to DG ( S654A ) littermates.
0.9957 In addition, muscles in DG ( S654A ) / CT transgenic mice had little or no evidence of muscular dystrophy when compared to ProteinDG ( S654A ) littermates.
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0.9948 These experiments demonstrate that the CT GalNAc transferase can affect the post - translational processing of Proteindystroglycan and the extent of muscular dystrophy even in muscles where the VIA4 - 1 antigen is not present.
0.9403 These experiments demonstrate that the ProteinCT GalNAc transferase can affect the post - translational processing of dystroglycan and the extent of muscular dystrophy even in muscles where the VIA4 - 1 antigen is not present.
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0.9995 Characterization of two novel proteins, NgRH1 and ProteinNgRH2 , structurally and biochemically homologous to the Nogo - 66 receptor.
0.9993 Characterization of two novel proteins, ProteinNgRH1 and NgRH2, structurally and biochemically homologous to the Nogo - 66 receptor.
0.9235 Characterization of two novel proteins, NgRH1 and NgRH2, structurally and biochemically homologous to the ProteinNogo - 66 receptor .
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0.9952 Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins ProteinNogo - A , oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.9863 Nogo - 66 receptor Protein( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.9735 Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein Protein( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.9712 ProteinNogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.9659 Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein Protein( MAG ) , and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.9487 Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, Proteinoligodendrocyte protein ( OMgp ) and myelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
0.8808 Nogo - 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin - associated proteins Nogo - A, oligodendrocyte protein ( OMgp ) and Proteinmyelin - associated glycoprotein ( MAG ), and mediates inhibition of axonal regeneration both in vitro and in vivo.
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0.9997 Through database searches, we have identified two novel proteins ( NgRH1 and NgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to ProteinNgR .
0.9997 Through database searches, we have identified two novel proteins ( NgRH1 and ProteinNgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to NgR.
0.9988 Through database searches, we have identified two novel proteins Protein( NgRH1 and NgRH2 ) that turned out to be homologous in their primary structures, biochemical properties and expression patterns to NgR.
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0.9995 Like ProteinNgR , the homologues contain eight leucine - rich repeats ( LRR ) flanked by a leucine - rich repeat C - terminus ( LRRCT ) and a leucine - rich repeat N - terminus ( LRRNT ), and also have a C - terminal GPI signal sequence.
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0.9997 Northern blot analysis showed predominant expression of NgRH1 and ProteinNgRH2 mRNA in the brain.
0.9996 Northern blot analysis showed predominant expression of ProteinNgRH1 and NgRH2 mRNA in the brain.
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0.9990 NgRH1 and ProteinNgRH2 were detected on the cell surface of recombinant cell lines as N - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes.
0.9985 ProteinNgRH1 and NgRH2 were detected on the cell surface of recombinant cell lines as N - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes.
0.9899 NgRH1 and NgRH2 were detected on the cell surface of recombinant cell lines as GlycosylationN - glycosylated GPI anchored proteins and, consistent with other GPI anchored proteins, were localized within the lipid rafts of cellular membranes.
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0.9997 In addition, an N - terminal proteolytic fragment of ProteinNgR comprising the majority of the ectodomain was found to be constitutively secreted from cells.
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0.9992 Our data indicate that NgR, NgRH1 and ProteinNgRH2 constitute a novel receptor protein family, which may play related roles within the CNS.
0.9986 Our data indicate that NgR, ProteinNgRH1 and NgRH2 constitute a novel receptor protein family, which may play related roles within the CNS.
0.9973 Our data indicate that ProteinNgR , NgRH1 and NgRH2 constitute a novel receptor protein family, which may play related roles within the CNS.
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0.9438 Synthesis of hydroxymethylglutathione from glutathione and L - serine catalyzed by Proteincarboxypeptidase Y .
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0.9779 We found that carboxypeptidase Y Protein( CPY ) , but not carboxypeptidase A, catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH.
0.8863 We found that Proteincarboxypeptidase Y ( CPY ), but not carboxypeptidase A, catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH.
0.8455 We found that carboxypeptidase Y ( CPY ), but not Proteincarboxypeptidase A , catalyzed hmGSH synthesis from glutathione and L - serine in vitro at acidic pH.
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0.9975 Transcriptional elongation by RNA polymerase II and Proteinhistone methylation.
0.9516 Transcriptional elongation by RNA polymerase II and histone Methylationmethylation .
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0.9981 In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone methylation by COMPASS, ProteinDot1p , and Set2 methyltransferases.
0.9981 In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to Proteinhistone methylation by COMPASS, Dot1p, and Set2 methyltransferases.
0.9981 In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone methylation by COMPASS, Dot1p, and ProteinSet2 methyltransferases.
0.5500 In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Methylationmethylation by COMPASS, Dot1p, and Set2 methyltransferases.
In this article, we will review the recent literature linking the key biochemical process of transcriptional elongation by RNA polymerase II to histone Catalysismethylation by COMPASS, Dot1p, and Set2 methyltransferases.
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0.9353 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and Proteinplatelet glycoprotein VI but not to alpha 2 beta 1.
0.7942 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 Proteinbeta 1 .
0.7669 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1.
0.7274 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 Proteinbeta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
0.7192 Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
0.9459 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1 .
0.9447 Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
0.7023 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to Proteinalpha 2 beta 1.
0.6902 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet Proteinglycoprotein VI but not to alpha 2 beta 1.
0.6827 Prolyl hydroxylation of collagen type I is required for efficient binding to Proteinintegrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
0.6570 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha 1 beta 1 and platelet glycoprotein VI but not to alpha Protein2 beta 1 .
0.5569 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin alpha Protein1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
0.5300 Prolyl hydroxylation of collagen type I is required for efficient binding to integrin Proteinalpha 1 beta 1 and platelet glycoprotein VI but not to alpha 2 beta 1.
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0.8100 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and alpha 2 Proteinbeta 1 .
0.6564 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1.
0.6361 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1.
0.6072 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 Proteinbeta 1 and alpha 2 beta 1.
0.9314 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1 .
0.9018 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1.
0.6696 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and alpha Protein2 beta 1 .
0.5961 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the Proteinintegrins alpha 1 beta 1 and alpha 2 beta 1.
0.5501 Collagen is a potent adhesive substrate for cells, an event essentially mediated by the integrins alpha 1 beta 1 and Proteinalpha 2 beta 1.
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0.8534 Collagen fibrils also bind to the integrin alpha 2 beta 1 and the Proteinplatelet receptor glycoprotein VI to activate and aggregate platelets.
0.8337 Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
0.7515 Collagen fibrils also bind to the integrin alpha 2 Proteinbeta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
0.9398 Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
0.8212 Collagen fibrils also bind to the Proteinintegrin alpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
0.6488 Collagen fibrils also bind to the integrin alpha Protein2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
0.6096 Collagen fibrils also bind to the integrin alpha 2 beta 1 and the platelet receptor Proteinglycoprotein VI to activate and aggregate platelets.
0.5837 Collagen fibrils also bind to the integrin alpha 2 beta 1 and the platelet Proteinreceptor glycoprotein VI to activate and aggregate platelets.
0.5626 Collagen fibrils also bind to the integrin Proteinalpha 2 beta 1 and the platelet receptor glycoprotein VI to activate and aggregate platelets.
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0.7679 We show that alpha 2 Proteinbeta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.7187 We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.6411 We show that alpha 2 beta 1 but not alpha 1 Proteinbeta 1 mediates cell adhesion to unhydroxylated collagen.
0.6122 We show that alpha 2 beta 1 but not Proteinalpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.9010 We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.8705 We show that alpha 2 beta 1 but not Proteinalpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.6512 We show that alpha Protein2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
0.6263 We show that Proteinalpha 2 beta 1 but not alpha 1 beta 1 mediates cell adhesion to unhydroxylated collagen.
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0.8606 Soluble recombinant alpha 1 Proteinbeta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
0.7338 Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
0.8975 Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
0.8135 Soluble recombinant alpha Protein1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
0.6925 Soluble recombinant Proteinalpha 1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
0.5248 Soluble recombinant alpha Protein1 beta 1 binding to unhydroxylated collagen is considerably reduced compared with bovine collagens, but binding can be restored by prolyl hydroxylation of recombinant collagen.
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0.9418 We also show that platelets use alpha 2 Proteinbeta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
0.8463 We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
0.9671 We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
0.9109 We also show that platelets use alpha Protein2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
0.8095 We also show that platelets use Proteinalpha 2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
0.6020 We also show that platelets use alpha Protein2 beta 1 to adhere to the unhydroxylated recombinant molecules, but the adhesion is weaker than on fully hydroxylated collagen, and the unhydroxylated collagen fibrils fail to aggregate platelets.
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0.9091 Prolyl hydroxylation is thus required for binding of collagen to Proteinplatelet glycoprotein VI and to cells by alpha 1 beta 1.
0.8324 Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by alpha 1 Proteinbeta 1 .
0.6804 Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1.
0.9264 Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1 .
0.7171 Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by alpha Protein1 beta 1 .
0.6073 Prolyl hydroxylation is thus required for binding of collagen to platelet glycoprotein VI and to cells by Proteinalpha 1 beta 1.
0.5952 Prolyl hydroxylation is thus required for binding of collagen to platelet Proteinglycoprotein VI and to cells by alpha 1 beta 1.
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0.9920 Mechanism, mutagenesis, and chemical rescue of a Proteinbeta - mannosidase from cellulomonas fimi.
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0.9940 The chemical mechanism of a retaining Proteinbeta - mannosidase from Cellulomonas fimi has been characterized through steady - state kinetic analyses with a range of substrates, coupled with chemical rescue studies on both the wild - type enzyme and mutants in which active site carboxyl groups have been replaced.
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0.9971 The tentative assignment of E429 as the acid - base catalyst of ProteinMan2A on the basis of sequence alignments with other family 2 glycosidases was confirmed by the increased turnover rate observed for the mutant E429A in the presence of azide and fluoride, leading to the production of beta - mannosyl azide and beta - mannosyl fluoride, respectively.
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0.9968 Substantial oxocarbenium ion character at the transition state was demonstrated by the alpha - deuterium kinetic isotope effect for ProteinMan2A E429A of alpha - D ( V ) = 1. 12 + / - 0. 01.
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0.9856 Likely involvement of acid / base catalysis was revealed by the pH dependence of k ( cat ) for ProteinMan2A E429A, which follows a bell - shaped profile described by pK ( a ) values of 6. 1 and 8. 4, substantially different from that of the wild - type enzyme.
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0.9930 The glycosidic bond cleaving activity of ProteinMan2A E519A and E519S nucleophile mutants is restored with azide and fluoride and appears to correlate with the corresponding " glycosynthase " activities.
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0.9983 The contribution of the substrate 2 - hydroxyl to stabilization of the ProteinMan2A glycosylation transition state ( DeltaDeltaG ( ) = 5. 1 kcal mol ( - 1 ) ) was probed using a 2 - deoxymannose substrate.
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0.7864 This value, surprisingly, is comparable to that found from equivalent studies with Proteinbeta - glucosidases despite the geometric differences at C - 2 and the importance of hydrogen bonding at that position.
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0.9896 Occurrence of O - linked Xyl - GlcNAc and EntityXyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom.
0.9890 Occurrence of O - linked EntityXyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom.
0.9839 Occurrence of O - linked Xyl - GlcNAc and Xyl - Glc disaccharides in Proteintrocarin , a factor Xa homolog from snake venom.
0.9321 Occurrence of O - linked Xyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a Proteinfactor Xa homolog from snake venom.
0.7677 Occurrence of GlycosylationO - linked Xyl - GlcNAc and Xyl - Glc disaccharides in trocarin, a factor Xa homolog from snake venom.
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0.9992 ProteinTrocarin is a 46515 - Da group D prothrombin - activating glycoprotein from the venom of the Australian elapid, Tropidechis carinatus.
0.9932 Trocarin is a 46515 - Da group D Proteinprothrombin - activating glycoprotein from the venom of the Australian elapid, Tropidechis carinatus.
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0.9985 Amino acid sequencing and functional characterization of Proteintrocarin demonstrated that it is a structural and functional homolog of mammalian blood coagulation factor ( F ) Xa.
0.6913 Amino acid sequencing and functional characterization of trocarin demonstrated that it is a structural and functional homolog of mammalian blood Proteincoagulation factor ( F ) Xa .
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0.9912 In this study we show that, in contrast to mammalian Xa, which is not Glycosylationglycosylated , trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.9650 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, Proteintrocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.9144 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an GlycosylationO - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.8990 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an GlycosylationN - linked carbohydrate oligosaccharide in its heavy chain.
0.8868 In this study we show that, in contrast to mammalian ProteinXa , which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.7687 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its Entityheavy chain .
0.7522 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked Entitycarbohydrate oligosaccharide in its heavy chain.
0.6818 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its Entitylight chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.6305 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked Entitycarbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.8622 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate Entityoligosaccharide in its heavy chain.
0.8159 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light Entitychain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.8087 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy Entitychain .
0.7069 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its Entityheavy chain.
0.6974 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate Entitymoiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.6749 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its light chain and an N - linked Entitycarbohydrate oligosaccharide in its heavy chain.
0.5696 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked Entitycarbohydrate moiety in its light chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
0.5134 In this study we show that, in contrast to mammalian Xa, which is not glycosylated, trocarin contains an O - linked carbohydrate moiety in its Entitylight chain and an N - linked carbohydrate oligosaccharide in its heavy chain.
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0.9855 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, EntityGlcNAc - , Xyl - Glc - and Glc - structures linked to Ser 52.
0.9813 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, EntityXyl - Glc - and Glc - structures linked to Ser 52.
0.9705 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of EntityXyl - GlcNAc - , GlcNAc -, Xyl - Glc - and Glc - structures linked to Ser 52.
0.9619 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and EntityGlc - structures linked to Ser 52.
0.9477 Mass spectrometry and sugar compositional analysis indicate that the GlycosylationO - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and Glc - structures linked to Ser 52.
0.8243 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and Glc - structures linked to EntitySer 52 .
0.7969 Mass spectrometry and sugar compositional analysis indicate that the O - linked carbohydrate moiety is a mixture of Xyl - GlcNAc -, GlcNAc -, Xyl - Glc - and EntityGlc - structures linked to Ser 52.
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0.9811 The N - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the Proteinprothrombin activator.
0.9423 The GlycosylationN - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator.
0.9020 The N - linked carbohydrate on EntityAsn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator.
0.7438 The N - linked Entitycarbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator.
0.5997 The N - linked carbohydrate on Asn 45 of the heavy chain is a sialylated, diantennary Entityoligosaccharide that is located at the lip of the active site of the prothrombin activator.
0.5575 The N - linked carbohydrate on EntityAsn 45 of the heavy chain is a sialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator.
The N - linked carbohydrate on Asn 45 of the heavy chain is a Entitysialylated, diantennary oligosaccharide that is located at the lip of the active site of the prothrombin activator.
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0.9825 The low density lipoprotein ( LDL ) receptor - related protein 1 Protein( LRP1 ) belongs to a growing number of cell surface proteins that undergo regulated proteolytic processing that culminates in the release of their intracellular domain ( ICD ) by the intramembranous protease gamma - secretase.
0.5787 The Proteinlow density lipoprotein ( LDL ) receptor - related protein 1 ( LRP1 ) belongs to a growing number of cell surface proteins that undergo regulated proteolytic processing that culminates in the release of their intracellular domain ( ICD ) by the intramembranous protease gamma - secretase.
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0.9970 Here we show that ProteinLRP1 is differentially glycosylated in a tissue - specific manner and that carbohydrate addition reduces proteolytic cleavage of the extracellular domain and, concomitantly, ICD release.
0.9955 Here we show that LRP1 is differentially Glycosylationglycosylated in a tissue - specific manner and that carbohydrate addition reduces proteolytic cleavage of the extracellular domain and, concomitantly, ICD release.
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0.9797 The apolipoprotein E ( apoE ) receptor - 2 Protein( apoER2 ) , another member of the LDL receptor family with functions in cellular signal transmission, also undergoes sequential proteolytic processing, resulting in intracellular domain release into the cytoplasm.
The Proteinapolipoprotein E ( apoE ) receptor - 2 ( apoER2 ), another member of the LDL receptor family with functions in cellular signal transmission, also undergoes sequential proteolytic processing, resulting in intracellular domain release into the cytoplasm.
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0.9980 The penultimate processing step also involves cleavage of the ProteinapoER2 extracellular domain.
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0.9695 The rate at which this cleavage step occurs is determined by the Glycosylationglycosylation state of the receptor, which in turn is regulated by the alternative splicing of an exon encoding several O - linked sugar attachment sites.
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0.9998 Inactivation of Proteinp16 gene in leukemia.
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0.9998 To determine the frequency of Proteinp16 gene inactivation in leukemia cells, and to evaluate their value in the prediction of their clinical outcome.
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0.9990 Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect Proteinp16 gene methylation. p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ).
0.9989 Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect Proteinp16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene methylation. p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ).
0.9989 Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene methylation. Proteinp16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ).
0.9972 Bone marrow or peripheral blood samples from 48 patients with leukemia were examined by multiplex polymerase chain reaction ( MPCR ) to detect p16 gene homozygous deletion, and restriction enzyme PCR to detect p16 gene DNA_methylationmethylation . p16 gene inactivation were detected in 10 of the 48 patients ( 20. 4 % ).
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0.9993 They were five patients with Proteinp16 homozygous deletion, and five patients with p16 methylation, respectively. p16 gene inactivation correlates with adverse prognosis features.
0.9981 They were five patients with p16 homozygous deletion, and five patients with p16 methylation, respectively. Proteinp16 gene inactivation correlates with adverse prognosis features.
0.9966 They were five patients with p16 homozygous deletion, and five patients with Proteinp16 methylation, respectively. p16 gene inactivation correlates with adverse prognosis features.
0.9877 They were five patients with p16 homozygous deletion, and five patients with p16 DNA_methylationmethylation , respectively. p16 gene inactivation correlates with adverse prognosis features.
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0.9998 The patients with p16 inactivation had poor response to chemotherapy, and had significantly shorter survival times than the patients in whom Proteinp16 gene was preserved ( P < 0. 001 ).
0.9998 The patients with Proteinp16 inactivation had poor response to chemotherapy, and had significantly shorter survival times than the patients in whom p16 gene was preserved ( P < 0. 001 ).
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0.9999 The inactivation of Proteinp16 gene play a key role in the pathogenesis and the progression of some leukemia.
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0.9998 The detection of Proteinp16 gene is reliable prognostic factor that predict shortened survival times.
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0.9955 A haploid affair : core Proteinhistone transitions during spermatogenesis.
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0.9968 Therefore, an analysis of the role of Proteinhistone variants and modifications in these processes may shed light upon the mechanisms involved and the control of chromatin structure in general.
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0.9946 Histone variants such as histone H3. 3, ProteinH2AX , and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9895 Histone variants such as histone H3. 3, H2AX, and ProteinmacroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9845 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of Proteinhistones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9843 ProteinHistone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9743 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, ProteinuH2B ) , and phosphorylation of histone H3 ( H3p ).
0.9689 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of Proteinhistone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9676 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and ProteinH2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9651 Histone variants such as Proteinhistone H3. 3 , H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9373 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), Ubiquitinationubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9341 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B Protein( uH2A , uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9341 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and Phosphorylationphosphorylation of histone H3 ( H3p ).
0.9327 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 Protein( acH4 ) , ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9241 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 Protein( H3p ) .
0.9062 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of Proteinhistone H3 ( H3p ).
0.8937 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated Acetylationacetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9158 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and ProteinH2B ( uH2A , uH2B ), and phosphorylation of histone H3 ( H3p ).
0.9029 Histone variants such as Proteinhistone H3 . 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.7177 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of Proteinhistones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.6610 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of histone H4 ( acH4 ), ubiquitination of histones ProteinH2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
0.6304 Histone variants such as histone H3. 3, H2AX, and macroH2A appear to play key roles in the various stages of spermiogenesis, in addition to the specifically modulated acetylation of Proteinhistone H4 ( acH4 ) , ubiquitination of histones H2A and H2B ( uH2A, uH2B ), and phosphorylation of histone H3 ( H3p ).
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0.9976 This review will examine recent discoveries concerning the role of Proteinhistone modifications and variants during meiosis and spermatogenesis.
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0.9982 HIF prolyl - hydroxylase 2 is the key oxygen sensor setting low steady - state levels of ProteinHIF - 1alpha in normoxia.
0.8177 ProteinHIF prolyl - hydroxylase 2 is the key oxygen sensor setting low steady - state levels of HIF - 1alpha in normoxia.
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0.9855 In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 Proteinubiquitin ligase complex containing the von Hippel - Lindau tumour suppressor protein ( pVHL ).
0.9764 In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von Hippel - Lindau tumour suppressor protein Protein( pVHL ) .
0.8452 In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the Proteinvon Hippel - Lindau tumour suppressor protein ( pVHL ).
0.7291 In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von ProteinHippel - Lindau tumour suppressor protein ( pVHL ).
0.6931 In normoxia, the HIF - alpha subunits are targeted for destruction by prolyl hydroxylation, a specific modification that provides recognition for the E3 ubiquitin ligase complex containing the von Hippel - Lindau Proteintumour suppressor protein ( pVHL ).
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0.9990 Three HIF prolyl - hydroxylases ( PHD1, Protein2 and 3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits.
0.9976 Three HIF prolyl - hydroxylases ( PHD1, 2 and Protein3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits.
0.9942 Three HIF prolyl - hydroxylases Protein( PHD1 , 2 and 3 ) were identified recently in mammals and shown to hydroxylate HIF - alpha subunits.
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0.9998 Here we show that specific'silencing'of ProteinPHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia.
0.9998 Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and ProteinPHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia.
0.9998 Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of ProteinPHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia.
0.9995 Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate HIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of ProteinHIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia.
0.9994 Here we show that specific'silencing'of PHD2 with short interfering RNAs is sufficient to stabilize and activate ProteinHIF - 1alpha in normoxia in all the human cells investigated.'Silencing'of PHD1 and PHD3 has no effect on the stability of HIF - 1alpha either in normoxia or upon re - oxygenation of cells briefly exposed to hypoxia.
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0.9997 We therefore conclude that, in vivo, PHDs have distinct assigned functions, ProteinPHD2 being the critical oxygen sensor setting the low steady - state levels of HIF - 1alpha in normoxia.
0.9993 We therefore conclude that, in vivo, PHDs have distinct assigned functions, PHD2 being the critical oxygen sensor setting the low steady - state levels of ProteinHIF - 1alpha in normoxia.
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0.9997 Interestingly, ProteinPHD2 is upregulated by hypoxia, providing an HIF - 1 - dependent auto - regulatory mechanism driven by the oxygen tension.
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0.9993 Insulation of the chicken beta - globin chromosomal domain from a chromatin - condensing protein, ProteinMENT .
0.9720 Insulation of the chicken Proteinbeta - globin chromosomal domain from a chromatin - condensing protein, MENT.
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0.9994 We mapped the topography of a terminal stage - specific chromatin - condensing protein, ProteinMENT , across the active chicken beta - globin domain.
0.9894 We mapped the topography of a terminal stage - specific chromatin - condensing protein, MENT, across the active chicken Proteinbeta - globin domain.
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0.9990 We observed two sharp transitions of ProteinMENT concentration coinciding with the beta - globin boundary elements.
0.9971 We observed two sharp transitions of MENT concentration coinciding with the Proteinbeta - globin boundary elements.
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0.9977 The ProteinMENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ).
0.9802 The MENT distribution profile was opposite to that of acetylated core Proteinhistones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ).
0.9703 The MENT distribution profile was opposite to that of Acetylationacetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 ( H3me2K9 ).
0.9696 The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 Methylationdimethylated at lysine 9 ( H3me2K9 ).
0.9544 The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of Proteinhistone H3 dimethylated at lysine 9 ( H3me2K9 ).
0.8819 The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at Entitylysine 9 ( H3me2K9 ).
0.5393 The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 Entity( H3me2K9 ) .
The MENT distribution profile was opposite to that of acetylated core histones but correlated with that of histone H3 dimethylated at lysine 9 Protein( H3me2K9 ) .
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0.9986 Ectopic ProteinMENT expression in NIH 3T3 cells caused a large - scale and specific remodeling of chromatin marked by H3me2K9.
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0.9990 ProteinMENT colocalized with H3me2K9 both in chicken erythrocytes and NIH 3T3 cells.
0.9532 MENT colocalized with ProteinH3me2K9 both in chicken erythrocytes and NIH 3T3 cells.
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0.9991 Mutational analysis of ProteinMENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone hyperacetylation on the MENT - induced chromatin remodeling in vivo.
0.9899 Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone hyperacetylation on the ProteinMENT - induced chromatin remodeling in vivo.
0.9848 Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of Proteinhistone hyperacetylation on the MENT - induced chromatin remodeling in vivo.
0.9657 Mutational analysis of MENT and experiments with deacetylase inhibitors revealed the essential role of the reaction center loop domain and an inhibitory affect of histone Acetylationhyperacetylation on the MENT - induced chromatin remodeling in vivo.
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0.9971 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by ProteinMENT , while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.9966 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by ProteinMENT .
0.9753 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of Proteinhistone H3 specifically restored chromatin self - association by MENT.
0.9649 In vitro, the elimination of the Proteinhistone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.9461 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with Methylationdimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.9369 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not Acetylationacetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.7865 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.6977 In vitro, the elimination of the histone H3 N - terminal peptide containing lysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated EntityN - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
0.6568 In vitro, the elimination of the histone H3 N - terminal peptide containing Entitylysine 9 by trypsin blocked chromatin self - association by MENT, while reconstitution with dimethylated but not acetylated N - terminal domain of histone H3 specifically restored chromatin self - association by MENT.
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0.9996 We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting ProteinMENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation.
0.9942 We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and Proteinhistone hyperacetylation.
0.9781 We suggest that Proteinhistone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation.
0.9725 We suggest that histone H3 modification at lysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone Acetylationhyperacetylation .
0.5107 We suggest that histone H3 modification at Entitylysine 9 directly regulates chromatin condensation by recruiting MENT to chromatin in a fashion that is spatially constrained from active genes by gene boundary elements and histone hyperacetylation.
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0.9996 Requirement for Proteinneo1p in retrograde transport from the Golgi complex to the endoplasmic reticulum.
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0.9993 ProteinNeo1p from Saccharomyces cerevisiae is an essential P - type ATPase and potential aminophospholipid translocase ( flippase ) in the Drs2p family.
0.9971 Neo1p from Saccharomyces cerevisiae is an essential P - type ATPase and potential aminophospholipid translocase ( flippase ) in the ProteinDrs2p family.
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0.9997 We have previously implicated ProteinDrs2p in protein transport steps in the late secretory pathway requiring ADP - ribosylation factor ( ARF ) and clathrin.
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0.9995 Here, we present evidence that epitope - tagged ProteinNeo1p localizes to the endoplasmic reticulum ( ER ) and Golgi complex and is required for a retrograde transport pathway between these organelles.
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0.9998 Using conditional alleles of ProteinNEO1 , we find that loss of Neo1p function causes cargo - specific defects in anterograde protein transport early in the secretory pathway and perturbs glycosylation in the Golgi complex.
0.9996 Using conditional alleles of NEO1, we find that loss of ProteinNeo1p function causes cargo - specific defects in anterograde protein transport early in the secretory pathway and perturbs glycosylation in the Golgi complex.
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0.9997 ProteinRer1 - GFP , a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalized to the vacuole in neo1 - ts at the nonpermissive temperature.
0.9994 Rer1 - GFP, a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalized to the vacuole in Proteinneo1 - ts at the nonpermissive temperature.
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0.9852 Recombinant ProteinL - ferritin showed less precipitation even above a pH of 8. 65.
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0.9962 ProteinHistone hyperacetylation in mitosis prevents sister chromatid separation and produces chromosome segregation defects.
0.9733 Histone Acetylationhyperacetylation in mitosis prevents sister chromatid separation and produces chromosome segregation defects.
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0.9936 Posttranslational modifications of core Proteinhistones contribute to driving changes in chromatin conformation and compaction.
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0.9982 Herein, we investigated the role of histone deacetylation on the mitotic process by inhibiting Proteinhistone deacetylases shortly before mitosis in human primary fibroblasts.
0.9976 Herein, we investigated the role of Proteinhistone deacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts.
0.8260 Herein, we investigated the role of histone Deacetylationdeacetylation on the mitotic process by inhibiting histone deacetylases shortly before mitosis in human primary fibroblasts.
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0.9981 Cells entering mitosis with hyperacetylated Proteinhistones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin.
0.9821 Cells entering mitosis with Acetylationhyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin.
0.9808 Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho ProteinH3 antibody, increased recruitment of protein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin.
Cells entering mitosis with hyperacetylated histones displayed altered chromatin conformation associated with decreased reactivity to the anti - Ser 10 phospho H3 antibody, increased recruitment of Proteinprotein phosphatase 1 - delta on mitotic chromosomes, and depletion of heterochromatin protein 1 from the centromeric heterochromatin.
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0.9980 Inhibition of Proteinhistone deacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation.
0.8839 Inhibition of histone Deacetylationdeacetylation before mitosis produced defective chromosome condensation and impaired mitotic progression in living cells, suggesting that improper chromosome condensation may induce mitotic checkpoint activation.
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0.9959 Lagging chromosomes consisting of single or paired sisters were also induced by the presence of hyperacetylated Proteinhistones , indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles.
0.9890 Lagging chromosomes consisting of single or paired sisters were also induced by the presence of Acetylationhyperacetylated histones, indicating that the less constrained centromeric organization associated with heterochromatin protein 1 depletion may promote the attachment of kinetochores to microtubules coming from both poles.
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0.9939 Hydroxylated kininogens and Proteinkinins .
0.9793 Hydroxylated Proteinkininogens and kinins.
0.8546 HydroxylationHydroxylated kininogens and kinins.
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0.9824 ProteinHydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with plasma kallikrein.
0.9182 Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with Proteinplasma kallikrein .
0.9063 Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human high molecular weight ( H ) kininogen with plasma Proteinkallikrein .
Hydroxyprolyl - 3 - bradykinin was identified in the digest of purified human Proteinhigh molecular weight ( H ) kininogen with plasma kallikrein.
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0.9069 Hydroxyproline was not detected in the heavy and light chains portions of ProteinH kininogen , although they include three possible sites for hydroxylation of proline by proline hydroxylase.
0.7060 Hydroxyproline was not detected in the heavy and light chains portions of H kininogen, although they include three possible sites for Hydroxylationhydroxylation of proline by proline hydroxylase.
0.5596 Hydroxyproline was not detected in the heavy and light chains portions of H Proteinkininogen , although they include three possible sites for hydroxylation of proline by proline hydroxylase.
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0.9973 The content of hydroxyprolyl - 3 - bradykinin in H kininogen from individual plasmas varied from 14 % to 64 % of total Proteinkinin .
0.9842 The content of Proteinhydroxyprolyl - 3 - bradykinin in H kininogen from individual plasmas varied from 14 % to 64 % of total kinin.
0.8891 The content of hydroxyprolyl - 3 - bradykinin in ProteinH kininogen from individual plasmas varied from 14 % to 64 % of total kinin.
0.5702 The content of hydroxyprolyl - 3 - bradykinin in H Proteinkininogen from individual plasmas varied from 14 % to 64 % of total kinin.
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0.9690 The present results and our previous results indicate that only Proteinkinin moity in H kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase.
0.8933 The present results and our previous results indicate that only kinin moity in ProteinH kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase.
0.6976 The present results and our previous results indicate that only kinin moity in H kininogen from human and monkey plasmas has been partially Hydroxylationhydroxylated post - translationally by proline - 4 - hydroxylase.
0.6174 The present results and our previous results indicate that only kinin moity in H kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by Proteinproline - 4 - hydroxylase .
0.5876 The present results and our previous results indicate that only kinin moity in H Proteinkininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase.
0.5086 The present results and our previous results indicate that only kinin moity in ProteinH kininogen from human and monkey plasmas has been partially hydroxylated post - translationally by proline - 4 - hydroxylase.
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0.9407 Purification and characterization of soluble forms of human and rat Proteinstem cell factor recombinantly expressed by Escherichia coli and by Chinese hamster ovary cells.
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0.9647 Stem cell factor Protein( SCF ) is a novel, early - acting hematopoietic factor.
0.6746 ProteinStem cell factor ( SCF ) is a novel, early - acting hematopoietic factor.
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0.9998 We have recombinantly expressed forms of human and rat ProteinSCF corresponding to the soluble, processed form in Escherichia coli and in Chinese hamster ovary ( CHO ) cells.
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0.9970 After expression in E. coli, folding and oxidation of the ProteinSCF polypeptides are required.
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0.9934 The ProteinSCFs expressed in CHO cells are secreted into the medium in active state and, like the natural SCF, are glycosylated.
0.9844 The SCFs expressed in CHO cells are secreted into the medium in active state and, like the natural ProteinSCF , are glycosylated.
0.9834 The SCFs expressed in CHO cells are secreted into the medium in active state and, like the natural SCF, are Glycosylationglycosylated .
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0.9993 Purification of the recombinant ProteinSCFs is described.
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0.9809 Inhibition of fusion by neutralizing monoclonal antibodies to the Proteinhaemagglutinin - neuraminidase glycoprotein of Newcastle disease virus.
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0.9728 The majority of neutralizing monoclonal antibodies ( MAbs ) to the Proteinhaemagglutinin - neuraminidase ( HN ) glycoprotein of Newcastle disease virus prevent attachment of the virus to cellular receptors and inhibits virion - induced fusion from without ( FFWO ) and fusion from within ( FFWI ) mediated by the virus glycoprotein - laden infected cell surface.
0.9529 The majority of neutralizing monoclonal antibodies ( MAbs ) to the haemagglutinin - neuraminidase Protein( HN ) glycoprotein of Newcastle disease virus prevent attachment of the virus to cellular receptors and inhibits virion - induced fusion from without ( FFWO ) and fusion from within ( FFWI ) mediated by the virus glycoprotein - laden infected cell surface.
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0.9948 For these antibodies, the inhibition of fusion is presumed to be the result of the prevention of ProteinHN - mediated bridging of potential fusion partners.
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0.9972 This suggests that the requirement for ProteinHN may be different in the two modes of fusion.
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0.9983 The epitopes recognized by MAbs to sites 3 and 4 have been delineated by the identification of individual nucleotide substitutions in the ProteinHN genes of neutralization escape variants.
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0.9536 Some of the deduced amino acid substitutions result in additional N - linked glycosylation sites in ProteinHN , which are utilized and presumably account for the escape from neutralization.
0.8201 Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization.
0.8191 Some of the deduced amino acid substitutions result in additional N - linked glycosylation sites in HN, which are Glycosylationutilized and presumably account for the escape from neutralization.
0.8283 Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization.
0.7204 Some of the deduced amino acid substitutions result in additional N - linked Entityglycosylation sites in HN, which are utilized and presumably account for the escape from neutralization.
0.6617 Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization.
0.4769 Some of the deduced amino acid substitutions result in additional EntityN - linked glycosylation sites in HN, which are utilized and presumably account for the escape from neutralization.
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0.9976 The influence of N - linked glycosylation on the antigenicity and immunogenicity of rubella virus ProteinE1 glycoprotein.
0.8220 The influence of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein.
0.8842 The influence of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of rubella virus E1 glycoprotein.
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0.9992 Rubella virus ProteinE1 glycoprotein contains three functional N - linked glycosylation sites.
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0.9989 The role of N - linked glycosylation on the antigenicity and immunogenicity of ProteinE1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants.
0.9953 The role of N - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing ProteinE1 glycosylation mutants.
0.8824 The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants.
0.8918 The role of N - linked Glycosylationglycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants.
0.7445 The role of GlycosylationN - linked glycosylation on the antigenicity and immunogenicity of E1 glycoprotein was studied using vaccinia recombinants expressing E1 glycosylation mutants.
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0.9990 Expressed E1 glycosylation mutant proteins were recognized by a panel of E1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on ProteinE1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies.
0.9989 Expressed E1 glycosylation mutant proteins were recognized by a panel of ProteinE1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on E1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies.
0.9976 Expressed ProteinE1 glycosylation mutant proteins were recognized by a panel of E1 - specific monoclonal antibodies in radioimmunoprecipitation, immunofluorescence, and immunoblotting, indicating that carbohydrate side chains on E1 are not involved in the constitution of epitopes recognized by these monoclonal antibodies.
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0.9987 This observation was further supported by the fact that removal of oligosaccharides on E1 by glycosidase digestion did not significantly change the antigenicity of ProteinE1 .
0.9968 This observation was further supported by the fact that removal of oligosaccharides on ProteinE1 by glycosidase digestion did not significantly change the antigenicity of E1.
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0.9974 All the glycosylation mutants were capable of eliciting anti - RV ProteinE1 antibodies.
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0.9982 Our findings suggest that although carbohydrate on E1 is not directly involved in the antigenic structures of ProteinE1 , it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on E1.
0.9982 Our findings suggest that although carbohydrate on ProteinE1 is not directly involved in the antigenic structures of E1, it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on E1.
0.9979 Our findings suggest that although carbohydrate on E1 is not directly involved in the antigenic structures of E1, it is important in maintaining proper protein folding and stable conformation for expression of immunological epitopes on ProteinE1 .
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0.9534 GlycosylationGlycosylation of the interleukin - 1 receptor type I is required for optimal binding of interleukin - 1.
0.8109 Glycosylation of the Proteininterleukin - 1 receptor type I is required for optimal binding of interleukin - 1.
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0.9895 To determine the role of Glycosylationglycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1.
0.9695 To determine the role of glycosylation of the IL - 1 receptor type I Protein( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1.
0.9090 To determine the role of glycosylation of the ProteinIL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1.
0.8954 To determine the role of glycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of IL - 1, we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for ProteinIL - 1 .
0.6039 To determine the role of glycosylation of the IL - 1 receptor type I ( IL - 1RtI ) in the binding and function of ProteinIL - 1 , we used four plant lectins and glycosidase treatment on two different T - cell lines ( EL4 - 6. 1 and D10S ) and expressing high number of binding sites for IL - 1.
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0.9197 The lectins wheat germ agglutinin, phytohemagglutinin, and Proteinconcanavalin A inhibited in a dose - response manner the IL - 1 - induced proliferation of D10S cells.
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0.9902 Digestion by N - glycosidase significantly decreased the capacity of cells to bind IL - 1, and reduced by approximately 20, 000 D the M ( r ) of the ProteinIL - 1RtI .
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0.9839 This study demonstrates that Glycosylationglycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.9773 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of Glycosylationglycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.9554 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.9376 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked Entitycarbohydrates , that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.7725 This study demonstrates that glycosylation of the extracellular domain of the ProteinIL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.9880 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of ProteinIL - 1 to its type I receptor.
0.9640 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked Glycosylationglycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.8293 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to N - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this GlycosylationN - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
0.4637 This study demonstrates that glycosylation of the extracellular domain of the IL - 1RtI is due to GlycosylationN - linked carbohydrates, that the degree of glycosylation can vary in cells of different lineage, and that this N - linked glycosylation appears to be essential for optimal binding and activity of IL - 1 to its type I receptor.
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0.9991 Expression of ProteinCpgp40 / 15 in Toxoplasma gondii : a surrogate system for the study of Cryptosporidium glycoprotein antigens.
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0.9997 The glycoprotein products of the Cpgp40 / 15 gene, gp40 and Proteingp15 , are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies.
0.9996 The glycoprotein products of the Cpgp40 / 15 gene, Proteingp40 and gp15, are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies.
0.9990 The glycoprotein products of the ProteinCpgp40 / 15 gene, gp40 and gp15, are involved in C. parvum sporozoite attachment to and invasion of host cells and, as such, may be good targets for anticryptosporidial therapies.
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0.9575 However, the function of these antigens appears to be dependent on the presence of multiple O - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants.
0.9502 However, the function of these antigens appears to be dependent on the presence of multiple GlycosylationO - linked alpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants.
0.9233 However, the function of these antigens appears to be dependent on the presence of multiple O - linked alpha - N - acetylgalactosamine Entity( alpha - GalNAc ) determinants.
0.6846 However, the function of these antigens appears to be dependent on the presence of multiple O - linked Entityalpha - N - acetylgalactosamine ( alpha - GalNAc ) determinants.
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0.9989 As a unique approach to this problem, the ProteinCpgp40 / 15 gene was transiently expressed in Toxoplasma gondii, and the expressed recombinant glycoproteins were characterized.
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0.9998 Antisera to gp40 and Proteingp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1.
0.9996 Antisera to gp40 and gp15 reacted with the surface membranes of tachyzoites expressing the ProteinCpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1.
0.9996 Antisera to Proteingp40 and gp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein SAG1.
0.9995 Antisera to gp40 and gp15 reacted with the surface membranes of tachyzoites expressing the Cpgp40 / 15 construct, and this reactivity colocalized with that of antiserum to the T. gondii surface protein ProteinSAG1 .
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0.9981 Surface membrane localization was dependent on the presence of the glycophosphatidylinositol anchor attachment site present in the Proteingp15 coding sequence.
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0.9955 The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant Proteingp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase.
0.9929 The presence of terminal O - linked Entityalpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase.
0.9624 The presence of terminal GlycosylationO - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase.
0.9794 The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes alpha - GalNAc residues, and digestion with Proteinalpha - N - acetylgalactosaminidase .
0.7244 The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes Entityalpha - GalNAc residues, and digestion with alpha - N - acetylgalactosaminidase.
0.5534 The presence of terminal O - linked alpha - GalNAc determinants on the T. gondii recombinant gp40 was confirmed by reactivity with Helix pomatia lectin and the monoclonal antibody 4E9, which recognizes Entityalpha - GalNAc residues , and digestion with alpha - N - acetylgalactosaminidase.
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0.9995 In addition to appropriate localization and glycosylation, T. gondii apparently processes the gp40 / 15 precursor into the gp40 and Proteingp15 component glycopolypeptides, albeit inefficiently.
0.9990 In addition to appropriate localization and glycosylation, T. gondii apparently processes the gp40 / 15 precursor into the Proteingp40 and gp15 component glycopolypeptides, albeit inefficiently.
0.9982 In addition to appropriate localization and glycosylation, T. gondii apparently processes the Proteingp40 / 15 precursor into the gp40 and gp15 component glycopolypeptides, albeit inefficiently.
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0.9962 Aberrant methylation of ProteinDAP - kinase in therapy - related acute myeloid leukemia and myelodysplastic syndromes.
0.9670 Aberrant DNA_methylationmethylation of DAP - kinase in therapy - related acute myeloid leukemia and myelodysplastic syndromes.
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0.9698 Death - associated protein kinase Protein( DAP - kinase ) , a proapoptotic serine / threonine kinase, is a candidate tumor suppressor gene.
0.8802 ProteinDeath - associated protein kinase ( DAP - kinase ), a proapoptotic serine / threonine kinase, is a candidate tumor suppressor gene.
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0.9948 We studied the methylation status of ProteinDAP - kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia ( AML ) and 34 with a myelodysplastic syndrome ( MDS ) at the time of initial diagnosis by polymerase chain reaction ( PCR ).
0.9888 We studied the DNA_methylationmethylation status of DAP - kinase of 194 bone marrow samples from 160 patients with acute myeloid leukemia ( AML ) and 34 with a myelodysplastic syndrome ( MDS ) at the time of initial diagnosis by polymerase chain reaction ( PCR ).
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0.9984 Hypermethylation of ProteinDAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of DAP - kinase expression ( P =. 008 ).
0.9769 DNA_methylationHypermethylation of DAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of DAP - kinase expression ( P =. 008 ).
0.8817 Hypermethylation of DAP - kinase was present in 27. 5 % ( 44 of 160 ) of AML and in 47 % ( 16 of 34 ) of MDS specimens and significantly correlated to loss of ProteinDAP - kinase expression ( P =. 008 ).
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0.9871 ProteinDAP - kinase hypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis ( P =. 002 ) and with the presence of cytogenetic abnormalities ( P =. 02 ).
0.9825 DAP - kinase DNA_methylationhypermethylation in AML was associated with myelodysplastic changes in the bone marrow at the time of the initial diagnosis ( P =. 002 ) and with the presence of cytogenetic abnormalities ( P =. 02 ).
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0.9987 Alteration in the apoptotic response due to the loss of ProteinDAP - kinase function may be an early event in the transformation pathway to secondary leukemia via myelodysplasia.
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0.9979 DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 promoter hypermethylation, and ProteinCTNNB - 1 mutations.
0.9890 DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 Entitypromoter hypermethylation, and CTNNB - 1 mutations.
0.9818 DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), MLH - 1 promoter DNA_methylationhypermethylation , and CTNNB - 1 mutations.
0.9682 DNA from paraffin - embedded tissue of 6 APAs was evaluated for microsatellite instability ( MI ), ProteinMLH - 1 promoter hypermethylation, and CTNNB - 1 mutations.
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0.9992 Tissue sections were also subjected to MLH - 1, ProteinMSH - 2 , and beta - catenin immunostaining.
0.9981 Tissue sections were also subjected to MLH - 1, MSH - 2, and Proteinbeta - catenin immunostaining.
0.9925 Tissue sections were also subjected to ProteinMLH - 1 , MSH - 2, and beta - catenin immunostaining.
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0.9870 Two tumors exhibited ProteinMLH - 1 promoter hypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism.
0.9864 Two tumors exhibited MLH - 1 promoter DNA_methylationhypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism.
0.9824 Two tumors exhibited MLH - 1 Entitypromoter hypermethylation and showed focal negative MHL - 1 immunostaining ; 1 of these showed marked architectural complexity and cellular pleomorphism.
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0.9996 Five cases presented Proteinbeta - catenin nuclear immunoreactivity, but none of them had CTNNB - 1 mutations.
0.9971 Five cases presented beta - catenin nuclear immunoreactivity, but none of them had ProteinCTNNB - 1 mutations.
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0.9910 Some APAs exhibit MLH - 1 promoter DNA_methylationhypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma.
0.9863 Some APAs exhibit ProteinMLH - 1 promoter hypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma.
0.9695 Some APAs exhibit MLH - 1 Entitypromoter hypermethylation with focal lack of MLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma.
0.8882 Some APAs exhibit MLH - 1 promoter hypermethylation with focal lack of ProteinMLH - 1 immunostaining, a molecular abnormality involved in the transition from complex atypical hyperplasia to endometrioid adenocarcinoma.
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0.9941 A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair EntityPro - 564 hydroxylation.
0.9544 A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair Pro - 564 Hydroxylationhydroxylation .
0.9011 A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of hypoxia inducible factor - 1alpha Protein( HIF - 1alpha ) does not impair Pro - 564 hydroxylation.
0.8000 A common polymorphism in the oxygen - dependent degradation ( ODD ) domain of Proteinhypoxia inducible factor - 1alpha ( HIF - 1alpha ) does not impair Pro - 564 hydroxylation.
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0.9968 Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved proline residues at positions 402 and 564 in ProteinHIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain.
0.9745 Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on Hydroxylationhydroxylation of two conserved proline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain.
0.8789 Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain.
0.6517 Under normoxic conditions, the alpha subunit of HIF is rapidly degraded in a manner dependent on hydroxylation of two conserved Entityproline residues at positions 402 and 564 in HIF - 1alpha in the oxygen - dependent degradation ( ODD ) domain.
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0.9993 This allows subsequent recognition by the von Hippel - Lindau ( VHL ) tumor suppressor protein, which targets HIF for degradation by the Proteinubiquitin - proteasome pathway.
0.8779 This allows subsequent recognition by the von Hippel - Lindau Protein( VHL ) tumor suppressor protein, which targets HIF for degradation by the ubiquitin - proteasome pathway.
This allows subsequent recognition by the Proteinvon Hippel - Lindau ( VHL ) tumor suppressor protein, which targets HIF for degradation by the ubiquitin - proteasome pathway.
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0.9610 Under hypoxic conditions, prolyl hydroxylation of HIF is inhibited, allowing it to escape ProteinVHL - mediated degradation.
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0.9959 The transcriptional regulation of the Proteinerythropoietin gene by HIF raises the possibility that HIF may play a role in disorders of erythropoiesis, such as idiopathic erythrocytosis ( IE ).
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0.9998 RESULTS : Patients with IE were screened for changes in the ProteinHIF - 1alpha coding sequence, and a change in the ODD domain that converts Pro - 582 to Ser was identified in several patients.
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0.9946 CONCLUSION : The Pro582Ser change represents a common polymorphism of ProteinHIF - 1alpha that does not impair HIF - 1alpha prolyl hydroxylation.
0.9924 CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair ProteinHIF - 1alpha prolyl hydroxylation.
0.9489 CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair HIF - 1alpha prolyl Hydroxylationhydroxylation .
0.8726 CONCLUSION : The Pro582Ser change represents a common polymorphism of HIF - 1alpha that does not impair HIF - 1alpha Entityprolyl hydroxylation.
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0.9993 Although the Pro582Ser polymorphism is located in the ODD domain of HIF - 1alpha it does not diminish the association of HIF - 1alpha with ProteinVHL .
0.9993 Although the Pro582Ser polymorphism is located in the ODD domain of HIF - 1alpha it does not diminish the association of ProteinHIF - 1alpha with VHL.
0.9988 Although the Pro582Ser polymorphism is located in the ODD domain of ProteinHIF - 1alpha it does not diminish the association of HIF - 1alpha with VHL.
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0.9959 Expression of Proteinhistone acetyltransferases was down - regulated in poly ( ADP - ribose ) polymerase - 1 - deficient murine cells.
0.9189 Expression of histone acetyltransferases was down - regulated in Proteinpoly ( ADP - ribose ) polymerase - 1 - deficient murine cells.
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0.9774 NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout Protein( PARP - 1 - / - ) mice.
0.8555 NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from Proteinpoly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout ( PARP - 1 - / - ) mice.
0.9747 NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout Protein( PARP - 1 - / - ) mice.
0.9455 NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 ( PARP - 1 ) - knockout ( PARP - 1 Protein- / - ) mice.
NF - kappaB - dependent, as well as human immunodeficiency virus type - 1 ( HIV - 1 ) long terminal repeat ( LTR ) - dependent, reporter gene expression was significantly impaired in cells derived from poly ( ADP - ribose ) polymerase - 1 Protein( PARP - 1 ) - knockout ( PARP - 1 - / - ) mice.
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0.9983 In addition, the level of protein acetylation was markedly lower in ProteinPARP - 1 - / - cells than control ( PARP - 1 + / + ) cells.
0.9866 In addition, the level of protein acetylation was markedly lower in PARP - 1 - / - cells than control Protein( PARP - 1 + / + ) cells.
0.5370 In addition, the level of protein Acetylationacetylation was markedly lower in PARP - 1 - / - cells than control ( PARP - 1 + / + ) cells.
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0.9995 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), Proteinp300 , cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.9991 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in ProteinPARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.9990 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with ProteinPARP - 1 + / + cells.
0.9936 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor Protein( PCAF ) , were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.9929 Surprisingly, the expression levels of Proteinhistone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.9807 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein Protein( CBP ) , and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.9652 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and Proteinp300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.8667 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, ProteincAMP response element - binding protein - binding protein ( CBP ), and p300 / CBP - associated factor ( PCAF ), were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
0.5825 Surprisingly, the expression levels of histone acetyltransferases ( HATs ), p300, cAMP response element - binding protein - binding protein ( CBP ), and Proteinp300 / CBP - associated factor ( PCAF ) , were significantly reduced in PARP - 1 - / - cells, as compared with PARP - 1 + / + cells.
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0.9987 These results suggest that ProteinPARP - 1 is required for the proper expression of particular HATs.
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0.9992 Since p300 and CBP are coactivators of NF - kappaB, we propose here that ProteinPARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs.
0.9989 Since p300 and ProteinCBP are coactivators of NF - kappaB, we propose here that PARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs.
0.9982 Since Proteinp300 and CBP are coactivators of NF - kappaB, we propose here that PARP - 1 participates in NF - kappaB - dependent transcription by means of maintaining the expression of HATs.
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0.9693 The ITIM - bearing ProteinCLECSF6 ( DCIR ) is down - modulated in neutrophils by neutrophil activating agents.
0.9686 The ITIM - bearing CLECSF6 Protein( DCIR ) is down - modulated in neutrophils by neutrophil activating agents.
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0.9996 The recently discovered ProteinCLECSF6 protein displays the features of a receptor involved in the down - modulation of leukocyte activation.
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0.9984 Although ProteinCLECSF6 has been the focus of the interest of many researchers lately, a Western blot characterization of the protein is still lacking.
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0.9993 Four different ProteinCLECSF6 mRNA species have been discovered to date.
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0.9986 When deglycosylated, the protein displayed the molecular weight expected for the longest ProteinCLECSF6 form.
0.4936 When Deglycosylationdeglycosylated , the protein displayed the molecular weight expected for the longest CLECSF6 form.
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0.9869 We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor Protein( TNF - alpha ) , lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4.
0.9723 We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor Protein( GM - CSF ) , tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4.
0.9241 We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and Proteininterleukin ( IL ) - 4 .
0.9057 We showed a down - modulation of the expression of this protein in neutrophils treated with Proteingranulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4.
0.7893 We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), Proteintumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin ( IL ) - 4.
0.8551 We showed a down - modulation of the expression of this protein in neutrophils treated with granulocyte - macrophage - colony stimulating factor ( GM - CSF ), tumor necrosis factor ( TNF - alpha ), lipopolysaccharide ( LPS ), and interleukin Protein( IL ) - 4 .
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0.9997 This work supports the hypothesis that ProteinCLECSF6 is involved in the control of inflammation in neutrophils.
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0.9613 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing ProteinnptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region.
0.9420 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine DNA_methylationmethylation restricted to the 3'end and center part of the transcribed region.
0.7816 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the Entity3'end and center part of the transcribed region.
0.7225 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and Entitycenter part of the transcribed region.
0.5416 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII Protein( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region.
0.7828 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3 ' Entityend and center part of the transcribed region.
0.7353 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the Entity3 ' end and center part of the transcribed region.
0.7227 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and Entitycenter part of the transcribed region.
0.5820 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing ProteinnptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the transcribed region.
0.5382 Parental - silenced HeLo1 ( hemizygous for locus 1 ) plants show posttranscriptional silencing of the residing nptII ( neomycin phosphotransferase II ) transgene and cytosine methylation restricted to the 3'end and center part of the Entitytranscribed region .
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0.6076 Here, we report that with an increasing number of cell cycles, DNA methylation changes gradually, and methylation is introduced into the Entitypromoter during cell culture and more slowly in vegetatively propagated plants.
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0.9740 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine DNA_methylationmethylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the 35S promoter.
0.9654 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the ProteinnptII - transcribed region and the 35S promoter.
0.9293 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter .
0.8839 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5'end of the nptII - transcribed region and the 35S promoter.
0.9458 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the 35S Entitypromoter .
0.9054 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the Entity5 ' end of the nptII - transcribed region and the 35S promoter.
0.8944 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed region and the Entity35S promoter.
0.6277 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5 ' Entityend of the nptII - transcribed region and the 35S promoter.
0.5728 After 24 months of callus in vitro cultivation, an epigenetic variant, designated locus 1E, was obtained in which cytosine methylation of symmetrical ( CG and CNG ) sites was almost complete within the 5'end of the nptII - transcribed Entityregion and the 35S promoter.
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0.9692 Further, DNA_methylationmethylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1.
0.8032 Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1.
0.7896 Further, methylation of nonsymmetrical sites appeared de novo in the Entitypromoter , whereas this type of methylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1.
0.9536 Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of DNA_methylationmethylation was significantly reduced in the 3'end of the transcribed region when compared with locus 1.
0.6352 Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the 3'end of the Entitytranscribed region when compared with locus 1.
0.5083 Further, methylation of nonsymmetrical sites appeared de novo in the promoter, whereas this type of methylation was significantly reduced in the Entity3 ' end of the transcribed region when compared with locus 1.
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0.9989 The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the ProteinnptII gene, indicating that the methylated promoter became inactivated.
0.9927 The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the nptII gene, indicating that the methylated Entitypromoter became inactivated.
0.9706 The protein and steady - state RNA levels remained low in locus 1E, whereas with nuclear run - on assays, no detectable amounts of primary transcripts were found along the nptII gene, indicating that the DNA_methylationmethylated promoter became inactivated.
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0.9968 Frequent methylation of p16INK4A and Proteinp14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase.
0.9966 Frequent methylation of Proteinp16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase.
0.8214 Frequent DNA_methylationmethylation of p16INK4A and p14ARF genes implicated in the evolution of chronic myeloid leukaemia from its chronic to accelerated phase.
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0.9971 The frequency and mechanism of p16 ( INK4A ) and Proteinp14 ( ARF ) gene alterations were studied in cell samples from 30 patients with Philadelphia ( Ph ) chromosome - positive chronic myeloid leukaemia ( CML ), both at diagnosis and at the onset of the accelerated phase ( AP ) of the disease.
0.9964 The frequency and mechanism of Proteinp16 ( INK4A ) and p14 ( ARF ) gene alterations were studied in cell samples from 30 patients with Philadelphia ( Ph ) chromosome - positive chronic myeloid leukaemia ( CML ), both at diagnosis and at the onset of the accelerated phase ( AP ) of the disease.
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0.9950 No alterations in the Proteinp16 ( INK4A ) or p14 ( ARF ) genes were found in any of the chronic phase ( CP ) samples.
0.9935 No alterations in the p16 ( INK4A ) or Proteinp14 ( ARF ) genes were found in any of the chronic phase ( CP ) samples.
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0.9970 DNA sequencing analyses detected Proteinp16 ( INK4A ) or p14 ( ARF ) mutations in 17 AP samples.
0.9970 DNA sequencing analyses detected p16 ( INK4A ) or Proteinp14 ( ARF ) mutations in 17 AP samples.
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0.9930 Aberrant DNA_methylationmethylation of the p16 ( INK4A ) or p14 ( ARF ) promoters was found in 14 of 30 AP samples.
0.9839 Aberrant methylation of the p16 ( INK4A ) or Proteinp14 ( ARF ) promoters was found in 14 of 30 AP samples.
0.9797 Aberrant methylation of the Proteinp16 ( INK4A ) or p14 ( ARF ) promoters was found in 14 of 30 AP samples.
0.9729 Aberrant methylation of the p16 ( INK4A ) or p14 ( ARF ) Entitypromoters was found in 14 of 30 AP samples.
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0.9765 The most common situation was the simultaneous methylation of both Entitypromoters .
0.9643 The most common situation was the simultaneous DNA_methylationmethylation of both promoters.
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0.9933 Our data indicate that p16 ( INK4A ) and Proteinp14 ( ARF ) are primary targets for inactivation by promoter methylation in the acceleration of CML.
0.9919 Our data indicate that Proteinp16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by promoter methylation in the acceleration of CML.
0.9915 Our data indicate that p16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by Entitypromoter methylation in the acceleration of CML.
0.9585 Our data indicate that p16 ( INK4A ) and p14 ( ARF ) are primary targets for inactivation by promoter DNA_methylationmethylation in the acceleration of CML.
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0.9957 Transcriptional silencing of the Proteinp16 ( INK4A ) and p14 ( ARF ) genes may be important in the conversion of CML from the CP to the AP.
0.9926 Transcriptional silencing of the p16 ( INK4A ) and Proteinp14 ( ARF ) genes may be important in the conversion of CML from the CP to the AP.
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0.9996 mSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene Proteincad .
0.9996 mSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the ProteinMyc target gene cad.
0.9763 ProteinmSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad.
0.9317 mSin3A / histone deacetylase 2 - and PRMT5 - containing ProteinBrg1 complex is involved in transcriptional repression of the Myc target gene cad.
0.7093 ProteinmSin3A / histone deacetylase 2 - and PRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad.
0.6314 mSin3A / histone deacetylase 2 - and ProteinPRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad.
0.7867 mSin3A / histone deacetylase 2 - and ProteinPRMT5 - containing Brg1 complex is involved in transcriptional repression of the Myc target gene cad.
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0.9715 We have previously shown that subunits of the mSin3A / histone deacetylase 2 Protein( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes.
0.9288 We have previously shown that subunits of the ProteinmSin3A / histone deacetylase 2 ( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes.
0.6487 We have previously shown that subunits of the ProteinmSin3A / histone deacetylase 2 ( HDAC2 ) corepressor complex copurify with hSWI / SNF complexes.
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0.9999 Here we show that the type II arginine - specific methyltransferase ProteinPRMT5 , which is involved in cyclin E repression, can be found in association with Brg1 and hBrm - based hSWI / SNF complexes.
0.9998 Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in cyclin E repression, can be found in association with ProteinBrg1 and hBrm - based hSWI / SNF complexes.
0.9986 Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in cyclin E repression, can be found in association with Brg1 and ProteinhBrm - based hSWI / SNF complexes.
0.7728 Here we show that the type II arginine - specific methyltransferase PRMT5, which is involved in Proteincyclin E repression, can be found in association with Brg1 and hBrm - based hSWI / SNF complexes.
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0.9889 We also show that hSWI / SNF - associated ProteinPRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
0.9673 We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and ProteinH4 more efficiently than hyperacetylated histones H3 and H4.
0.9507 We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and ProteinH4 .
0.8992 We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated Proteinhistones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
0.8981 We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than Acetylationhyperacetylated histones H3 and H4.
0.8859 We also show that hSWI / SNF - associated PRMT5 can methylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated Proteinhistones H3 and H4.
0.5522 We also show that hSWI / SNF - associated PRMT5 can Methylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
0.8602 We also show that hSWI / SNF - associated PRMT5 can methylate Acetylationhypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
0.4086 We also show that hSWI / SNF - associated PRMT5 can Acetylationmethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
We also show that hSWI / SNF - associated PRMT5 can Catalysismethylate hypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
We also show that hSWI / SNF - associated PRMT5 can methylate Deacetylationhypoacetylated histones H3 and H4 more efficiently than hyperacetylated histones H3 and H4.
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0.9998 Protein - protein interaction studies indicate that PRMT5 and mSin3A interact with the same hSWI / SNF subunits as those targeted by Proteinc - Myc .
0.9997 Protein - protein interaction studies indicate that ProteinPRMT5 and mSin3A interact with the same hSWI / SNF subunits as those targeted by c - Myc.
0.9996 Protein - protein interaction studies indicate that PRMT5 and ProteinmSin3A interact with the same hSWI / SNF subunits as those targeted by c - Myc.
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0.9995 These observations prompted us to examine the expression profile of the Proteinc - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
0.9893 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase Protein( cad ) and nucleolin ( nuc ).
0.9884 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin Protein( nuc ) .
0.8008 These observations prompted us to examine the expression profile of the c - Myc target genes, Proteincarbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
0.7198 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and Proteinnucleolin ( nuc ).
0.6112 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate synthase - aspartate Proteincarbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
0.5662 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate Proteinsynthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
0.7418 These observations prompted us to examine the expression profile of the c - Myc target genes, Proteincarbamoyl - phosphate synthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
0.5126 These observations prompted us to examine the expression profile of the c - Myc target genes, carbamoyl - phosphate Proteinsynthase - aspartate carbamoyltransferase - dihydroorotase ( cad ) and nucleolin ( nuc ).
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0.9998 We found that Proteincad repression is altered in cells that express inactive Brg1 and in cells treated with the HDAC inhibitor depsipeptide.
0.9997 We found that cad repression is altered in cells that express inactive ProteinBrg1 and in cells treated with the HDAC inhibitor depsipeptide.
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0.9998 Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, HDAC2, and ProteinPRMT5 are directly recruited to the cad promoter.
0.9996 Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, ProteinHDAC2 , and PRMT5 are directly recruited to the cad promoter.
0.9995 Using chromatin immunoprecipitation assays, we found that Brg1, ProteinmSin3A , HDAC2, and PRMT5 are directly recruited to the cad promoter.
0.9994 Using chromatin immunoprecipitation assays, we found that ProteinBrg1 , mSin3A, HDAC2, and PRMT5 are directly recruited to the cad promoter.
0.9967 Using chromatin immunoprecipitation assays, we found that Brg1, mSin3A, HDAC2, and PRMT5 are directly recruited to the Proteincad promoter.
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0.9651 Centromere silencing and function in fission yeast is governed by the amino terminus of Proteinhistone H3 .
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0.9866 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and ProteinH4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ).
0.9522 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and Methylationmethylation of lysine 9 of histone H3 ( K9 - MeH3 ).
0.9332 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of Proteinhistones H3 and H4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ).
0.9282 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of Proteinhistone H3 ( K9 - MeH3 ).
0.9264 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by Acetylationhypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 ( K9 - MeH3 ).
0.8943 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ).
0.5115 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 Entity( K9 - MeH3 ) .
0.5391 BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of Entitylysine 9 of histone H3 ( K9 - MeH3 ).
BACKGROUND : Centromeric domains often consist of repetitive elements that are assembled in specialized chromatin, characterized by hypoacetylation of histones H3 and H4 and methylation of lysine 9 of histone H3 Protein( K9 - MeH3 ) .
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0.9991 Perturbation of this underacetylated state by transient treatment with histone deacetylase inhibitors leads to defective centromere function, correlating with delocalization of the heterochromatin protein ProteinSwi6 / HP1 .
0.9987 Perturbation of this underacetylated state by transient treatment with Proteinhistone deacetylase inhibitors leads to defective centromere function, correlating with delocalization of the heterochromatin protein Swi6 / HP1.
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0.9987 Likewise, deletion of the K9 - MeH3 methyltransferase ProteinClr4 / Suvar39 causes defective chromosome segregation.
0.9893 Likewise, deletion of the ProteinK9 - MeH3 methyltransferase Clr4 / Suvar39 causes defective chromosome segregation.
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0.9995 Here, we create fission yeast strains retaining one histone H3 and ProteinH4 gene ; the creation of these strains allows mutation of specific N - terminal tail residues and their role in centromeric silencing and chromosome stability to be investigated.
0.9899 Here, we create fission yeast strains retaining one Proteinhistone H3 and H4 gene ; the creation of these strains allows mutation of specific N - terminal tail residues and their role in centromeric silencing and chromosome stability to be investigated.
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0.9993 RESULTS : Reduction of ProteinH3 / H4 gene dosage to one - third does not affect cell viability or heterochromatin formation.
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0.9994 Mutation of lysines 9 or 14 or serine 10 within the amino terminus of histone H3 impairs centromere function, leading to defective chromosome segregation and ProteinSwi6 delocalization.
0.9658 Mutation of lysines 9 or 14 or serine 10 within the amino terminus of Proteinhistone H3 impairs centromere function, leading to defective chromosome segregation and Swi6 delocalization.
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0.9723 Surprisingly, silent centromeric chromatin does not require the conserved lysine 8 and 16 residues of Proteinhistone H4 .
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0.9989 CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous histone genes has only been performed in budding yeast, which lacks the Clr4 / Suvar39 histone methyltransferase and ProteinSwi6 / HP1 .
0.9976 CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous Proteinhistone genes has only been performed in budding yeast, which lacks the Clr4 / Suvar39 histone methyltransferase and Swi6 / HP1.
0.9228 CONCLUSIONS : To date, mutation of conserved N - terminal residues in endogenous histone genes has only been performed in budding yeast, which lacks the ProteinClr4 / Suvar39 histone methyltransferase and Swi6 / HP1.
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0.9839 We demonstrate the importance of conserved residues within the Proteinhistone H3 N terminus for the maintenance of centromeric heterochromatin in fission yeast.
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0.9493 In sharp contrast, mutation of two conserved lysines within the Proteinhistone H4 tail has no impact on the integrity of centromeric heterochromatin.
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0.9949 Our data highlight the striking divergence between the Proteinhistone tail requirements for the fission yeast and budding yeast silencing pathways.
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0.9844 Thermal stability and aggregation of sulfolobus solfataricus Proteinbeta - glycosidase are dependent upon the N - epsilon - methylation of specific lysyl residues : critical role of in vivo post - translational modifications.
0.9442 Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the N - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications.
0.6472 Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the MethylationN - epsilon - methylation of specific lysyl residues : critical role of in vivo post - translational modifications.
0.8880 Thermal stability and aggregation of sulfolobus solfataricus beta - glycosidase are dependent upon the N - epsilon - methylation of specific Entitylysyl residues : critical role of in vivo post - translational modifications.
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0.9784 The aim of this work is to clarify some effects of methylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, Methylationmethylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli.
0.9692 The aim of this work is to clarify some effects of methylation on the properties of Proteinbeta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli.
0.9608 The aim of this work is to clarify some effects of methylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its Methylationunmethylated counterpart, recombinantly expressed in Escherichia coli.
0.9157 The aim of this work is to clarify some effects of Methylationmethylation on the properties of beta - glycosidase from Sulfolobus solfataricus, by a structural comparison between the native, methylated protein and its unmethylated counterpart, recombinantly expressed in Escherichia coli.
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0.9969 However, the study of temperature perturbation by Fourier transform infrared spectroscopy and turbidimetry evidenced denaturation and aggregation events more pronounced in recombinant than in native Proteinbeta - glycosidase .
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0.9915 A computational analysis of Proteinbeta - glycosidase three - dimensional structure and comparisons with other proteins from S. solfataricus revealed analogies in the localization of methylation sites in terms of secondary structural elements and overall topology.
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0.9913 These observations suggest a role for the methylation of lysyl residues, located in selected domains, in the thermal stabilization of Proteinbeta - glycosidase from S. solfataricus.
0.9567 These observations suggest a role for the Methylationmethylation of lysyl residues, located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus.
0.9143 These observations suggest a role for the methylation of Entitylysyl residues , located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus.
0.6708 These observations suggest a role for the methylation of Entitylysyl residues, located in selected domains, in the thermal stabilization of beta - glycosidase from S. solfataricus.
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0.9632 Two pathways for PC biosynthesis are known in bacteria, the methylation pathway and the phosphatidylcholine synthase Protein( PCS ) pathway.
0.8586 Two pathways for PC biosynthesis are known in bacteria, the methylation pathway and the Proteinphosphatidylcholine synthase ( PCS ) pathway.
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0.9990 Using cell - free extracts, it was demonstrated that Sinorhizobium meliloti, Agrobacterium tumefaciens, Rhizobium leguminosarum, Bradyrhizobium japonicum, Mesorhizobium loti and Legionella pneumophila have both PMT and ProteinPCS activities.
0.9123 Using cell - free extracts, it was demonstrated that Sinorhizobium meliloti, Agrobacterium tumefaciens, Rhizobium leguminosarum, Bradyrhizobium japonicum, Mesorhizobium loti and Legionella pneumophila have both ProteinPMT and PCS activities.
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0.9995 Genes from M. loti and L. pneumophila encoding a ProteinPmt or a Pcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for Pcs activity have been identified.
0.9987 Genes from M. loti and L. pneumophila encoding a Pmt or a Pcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for ProteinPcs activity have been identified.
0.9986 Genes from M. loti and L. pneumophila encoding a Pmt or a ProteinPcs activity and the genes from P. aeruginosa and Borrelia burgdorferi responsible for Pcs activity have been identified.
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0.9992 However, important pathogens such as Brucella melitensis, P. aeruginosa and Borrelia burgdorferi seem to be exceptional as they possess only the ProteinPCS pathway for PC formation.
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0.9858 To validate our method, the product of human thiopurine methyltransferase Protein( TPMT , EC 2. 1. 1. 67 ) has been successfully identified from both an in vitro assay and a whole - cell assay.
0.9026 To validate our method, the product of human Proteinthiopurine methyltransferase ( TPMT, EC 2. 1. 1. 67 ) has been successfully identified from both an in vitro assay and a whole - cell assay.
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0.9297 Further analysis, including concanavalin A Protein( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides.
0.9002 Further analysis, including Proteinconcanavalin A ( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides.
0.7227 Further analysis, including concanavalin A Protein( Con A ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides.
0.5534 Further analysis, including concanavalin A ( Con ProteinA ) affinity chromatography, desialylation, desulphation, sequential exoglycosidase digestion and methylation, clarified the structures of the acidic oligosaccharides.
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0.9942 The ProteinMTHFR 677C > T polymorphism is associated with an increased risk of hepatocellular carcinoma in patients with alcoholic cirrhosis.
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0.9879 Methylenetetrahydrofolate reductase Protein( MTHFR ) , a key enzyme in folate metabolism, plays a major role in the provision of methyl groups for DNA methylation and in the production of dTMP for DNA synthesis.
0.9147 ProteinMethylenetetrahydrofolate reductase ( MTHFR ), a key enzyme in folate metabolism, plays a major role in the provision of methyl groups for DNA methylation and in the production of dTMP for DNA synthesis.
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0.9994 The aim of this study was to determine whether the ProteinMTHFR polymorphism is related to hepatocellular carcinoma ( HCC ) in patients with alcoholic cirrhosis.
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0.9995 ProteinMTHFR genotypes were determined in 300 liver transplant patients, 72 of whom had alcoholic cirrhosis with HCC and 122 of whom had alcoholic cirrhosis without HCC.
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0.9994 Among the group of patients transplanted for alcoholic cirrhosis, the frequency of ProteinMTHFR variants CC versus CT and TT was significantly higher in patients with HCC than in patients without macroscopic evidence of HCC ( P = 0. 02 ).
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0.9975 If we considered all the patients transplanted for HCC, the ProteinMTHFR CC genotype was significantly higher in patients who had developed HCC on alcoholic cirrhosis rather than on viral cirrhosis ( P = 0. 002 ) or on non - cirrhotic livers ( P = 0. 02 ).
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0.9920 These results suggest that the ProteinMTHFR CC genotype increases the risk to develop HCC in patients who consume a high alcohol diet.
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0.9998 ProteinMbd1 is recruited to both methylated and nonmethylated CpGs via distinct DNA binding domains.
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0.9998 ProteinMBD1 is a vertebrate methyl - CpG binding domain protein ( MBD ) that can bring about repression of methylated promoter DNA sequences.
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0.9999 Like other MBD proteins, ProteinMBD1 localizes to nuclear foci that in mice are rich in methyl - CpG.
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0.9998 In methyl - CpG - deficient mouse cells, however, ProteinMbd1 remains localized to heterochromatic foci whereas other MBD proteins become dispersed in the nucleus.
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0.9997 We find that ProteinMbd1a , a major mouse isoform, contains a CXXC domain ( CXXC - 3 ) that binds specifically to nonmethylated CpG, suggesting an explanation for methylation - independent localization.
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0.9998 Our findings indicate that ProteinMBD1 can interpret the CpG dinucleotide as a repressive signal in vivo regardless of its methylation status.
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0.9996 Recombinant human zona pellucida proteins ZP1, ZP2 and ProteinZP3 co - expressed in a human cell line.
0.9995 Recombinant human zona pellucida proteins ZP1, ProteinZP2 and ZP3 co - expressed in a human cell line.
0.9994 Recombinant human zona pellucida proteins ProteinZP1 , ZP2 and ZP3 co - expressed in a human cell line.
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0.9998 METHODS : The human embryonic kidney cell line 293T was employed to produce rhZP1, ProteinrhZP2 and rhZP3 proteins individually and together by co - expression.
0.9997 METHODS : The human embryonic kidney cell line 293T was employed to produce ProteinrhZP1 , rhZP2 and rhZP3 proteins individually and together by co - expression.
0.9994 METHODS : The human embryonic kidney cell line 293T was employed to produce rhZP1, rhZP2 and ProteinrhZP3 proteins individually and together by co - expression.
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0.9997 RESULTS : RhZP2 and rhZP3 were secreted into the culture medium, whereas ProteinrhZP1 was found only in the cell lysate.
0.9995 RESULTS : RhZP2 and ProteinrhZP3 were secreted into the culture medium, whereas rhZP1 was found only in the cell lysate.
0.9993 RESULTS : ProteinRhZP2 and rhZP3 were secreted into the culture medium, whereas rhZP1 was found only in the cell lysate.
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0.9998 Interestingly, when all zona pellucida proteins were co - expressed in the same cells, ProteinrhZP1 was also secreted into the culture medium.
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0.9992 CONCLUSION : RhZP1, ProteinrhZP2 and rhZP3 were successfully expressed in the human embryonic kidney cell line 293T.
0.9991 CONCLUSION : RhZP1, rhZP2 and ProteinrhZP3 were successfully expressed in the human embryonic kidney cell line 293T.
0.9983 CONCLUSION : ProteinRhZP1 , rhZP2 and rhZP3 were successfully expressed in the human embryonic kidney cell line 293T.
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0.9999 It appears that an interaction amongst these proteins may be required for release of ProteinrhZP1 from the cell.
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0.9983 Leu - 574 of human ProteinHIF - 1alpha is a molecular determinant of prolyl hydroxylation.
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ProteinHypoxia - inducible factor ( HIF ) - 1alpha , a master regulator of oxygen homeostasis, regulates genes crucial for cell growth and survival.
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0.9986 In normoxia, ProteinHIF - 1alpha is constantly degraded via the ubiquitin - proteasome pathway.
0.9977 In normoxia, HIF - 1alpha is constantly degraded via the Proteinubiquitin - proteasome pathway.
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0.9993 The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds ProteinHIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.9910 The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or EntityPro - 564 , both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.9771 The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated EntityPro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.9660 The von Hippel - Lindau ( VHL ) E3 Proteinubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.9576 The von Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of Hydroxylationhydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.9187 The von Hippel - Lindau Protein( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.7938 The Proteinvon Hippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
0.5841 The von ProteinHippel - Lindau ( VHL ) E3 ubiquitin ligase binds HIF - 1alpha through specific recognition of hydroxylated Pro - 402 or Pro - 564, both of which are modified by the oxygen - dependent HIF prolyl hydroxylases ( PHDs / HPHs ).
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0.9996 Despite the identification of a conserved Leu - X - X - Leu - Ala - Pro motif, the molecular requirement of ProteinHIF - 1alpha for PHDs / HPHs binding remains elusive.
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0.9959 Recently, we demonstrated that Leu - 574 of human ProteinHIF - 1alpha - - 10 residues downstream of Pro - 564 - - is essential for VHL recognition.
0.9952 Recently, we demonstrated that Leu - 574 of human HIF - 1alpha - - 10 residues downstream of Pro - 564 - - is essential for ProteinVHL recognition.
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0.9905 We show here that the role of Leu - 574 is to recruit ProteinPHD2 / HPH2 for Pro - 564 hydroxylation.
0.9351 We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for EntityPro - 564 hydroxylation.
0.6596 We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for Pro - 564 Hydroxylationhydroxylation .
We show here that the role of Leu - 574 is to recruit PHD2 / HPH2 for Pro - 564 Catalysishydroxylation .
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0.9870 An antibody specific for hydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated ProteinHIF - 1alpha to the total amount.
0.9752 An antibody specific for Hydroxylationhydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount.
0.9707 An antibody specific for hydroxylated Pro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the Hydroxylationhydroxylated HIF - 1alpha to the total amount.
0.9686 An antibody specific for hydroxylated EntityPro - 564 has been used to determine the hydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount.
0.9620 An antibody specific for hydroxylated Pro - 564 has been used to determine the Hydroxylationhydroxylation status ; mutation or deletion of Leu - 574 results in a significant decrease in the ratio of the hydroxylated HIF - 1alpha to the total amount.
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0.9767 The nine - residue spacing between Pro - 564 and Leu - 574 is not obligatory for prolyl Hydroxylationhydroxylation .
0.9677 The nine - residue spacing between Pro - 564 and Leu - 574 is not obligatory for Entityprolyl hydroxylation.
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0.9998 Furthermore, mutation of Leu - 574 disrupts the binding of ProteinPHD2 / HPH2 , a key prolyl hydroxylase for oxygen - dependent proteolysis of HIF - 1alpha.
0.9965 Furthermore, mutation of Leu - 574 disrupts the binding of PHD2 / HPH2, a key prolyl hydroxylase for oxygen - dependent proteolysis of ProteinHIF - 1alpha .
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0.9998 Hence, our findings indicate that Leu - 574 is essential for recruiting ProteinPHD2 / HPH2 , thereby providing a molecular basis for modulating HIF - 1alpha activity.
0.9995 Hence, our findings indicate that Leu - 574 is essential for recruiting PHD2 / HPH2, thereby providing a molecular basis for modulating ProteinHIF - 1alpha activity.
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0.9990 ProteinTransferrin microheterogeneity in fetal blood.
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0.9997 OBJECTIVES : To investigate the distribution of microheterogeneous subfractions of Proteintransferrin in fetal blood and the influence of highly sialylated transferrins on fetal growth.
0.9996 OBJECTIVES : To investigate the distribution of microheterogeneous subfractions of transferrin in fetal blood and the influence of highly sialylated Proteintransferrins on fetal growth.
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0.9974 STUDY METHOD : Serum Proteintransferrin concentrations were determined by a standard turbidimetric assay.
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0.9993 Microheterogeneous Proteintransferrin subfractions were assessed by crossed immunoisoelectric focusing.
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0.9990 RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated Proteintransferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women.
0.9989 RESULTS : In normal term infants, total serum Proteintransferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women.
0.9983 RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated Proteintransferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women.
0.9975 RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = Protein5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and 1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women.
0.9891 RESULTS : In normal term infants, total serum transferrin concentrations and percent distribution of highly sialylated transferrins ( > or = 5 - sialo - transferrins ) were markedly lower ; the percent distributions of hyposialylated transferrins ( 0 - and Protein1 - sialo - transferrins ) were apparently higher than those in non - pregnant and pregnant women.
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0.9995 There was no significant positive correlation between the serum concentrations of total Proteintransferrin or highly sialylated transferrins in infants'blood and birth weights ( r = 0. 187, p = 0. 582 ; r = 0. 374, p = 0. 257, respectively ).
0.9993 There was no significant positive correlation between the serum concentrations of total transferrin or highly sialylated Proteintransferrins in infants'blood and birth weights ( r = 0. 187, p = 0. 582 ; r = 0. 374, p = 0. 257, respectively ).
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0.9995 CONCLUSION : The Proteintransferrin microheterogeneity pattern shifted towards reduced glycosylation and sialylation in addition to a decrease in total transferrin concentration in fetal blood compared to that of non - pregnant and pregnant women.
0.9990 CONCLUSION : The transferrin microheterogeneity pattern shifted towards reduced glycosylation and sialylation in addition to a decrease in total Proteintransferrin concentration in fetal blood compared to that of non - pregnant and pregnant women.
0.9738 CONCLUSION : The transferrin microheterogeneity pattern shifted towards reduced Glycosylationglycosylation and sialylation in addition to a decrease in total transferrin concentration in fetal blood compared to that of non - pregnant and pregnant women.
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0.9996 The concentrations of serum total Proteintransferrin and the highly sialylated transferrins in fetal blood, if higher than a certain level, did not seem to have any influence on normal fetal growth.
0.9993 The concentrations of serum total transferrin and the highly sialylated Proteintransferrins in fetal blood, if higher than a certain level, did not seem to have any influence on normal fetal growth.
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0.9742 Heterochromatin and Methylationtri - methylated lysine 20 of histone H4 in animals.
0.9268 Heterochromatin and tri - methylated lysine 20 of Proteinhistone H4 in animals.
0.8498 Heterochromatin and tri - methylated Entitylysine 20 of histone H4 in animals.
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0.9874 MethylationTri - methylated lysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
0.8946 Tri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
0.8809 Tri - methylated lysine 20 on Proteinhistone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
0.6483 Tri - methylated lysine 20 on histone H4 Protein( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
0.5268 Tri - methylated Entitylysine 20 on histone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
0.5082 Tri - methylated lysine 20 on Proteinhistone H4 ( Me ( 3 ) K20H4 ) is a marker of constitutive heterochromatin in murine interphase and metaphase cells.
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0.9916 Heterochromatin marked by ProteinMe ( 3 ) K20H4 replicates late during S phase of the cell cycle.
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0.9752 Serum starvation increases the number of cells that exhibit high levels of ProteinMe ( 3 ) K20H4 at constitutive heterochromatin.
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0.9932 ProteinMe ( 3 ) K20H4 is also present at the centromeric heterochromatin of most meiotic chromosomes during spermatogenesis and at the pseudoautosomal region, as well as at some telomeres.
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0.9655 During murine embryogenesis the maternal pronucleus contains Me ( 3 ) K20H4 ; ProteinMe ( 3 ) K20H4 is absent from the paternal pronucleus.
0.9477 During murine embryogenesis the maternal pronucleus contains ProteinMe ( 3 ) K20H4 ; Me ( 3 ) K20H4 is absent from the paternal pronucleus.
0.9399 During murine embryogenesis the maternal pronucleus contains ProteinMe ( 3 ) K20H4 ; Me ( 3 ) K20H4 is absent from the paternal pronucleus.
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0.9936 On Drosophila polytene chromosomes ProteinMe ( 3 ) K20H4 is present in a'punctate pattern'at many chromosomal bands, including the chromocenter.
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0.9988 We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and ProteinH4 .
0.9911 We also present evidence that ProteinMe ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4.
0.9697 We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between Proteinhistones H3 and H4.
0.6694 We also present evidence that Me ( 3 ) K20H4 is dependent upon ProteinH3 - specific Suv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4.
0.6830 We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific ProteinSuv ( 3 ) 9 histone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4.
0.6558 We also present evidence that Me ( 3 ) K20H4 is dependent upon H3 - specific Suv ( 3 ) 9 Proteinhistone methyltransferase activity, suggesting that there may be'epigenetic cross - talk'between histones H3 and H4.
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0.9991 The Proteinhistone modification pattern of active genes revealed through genome - wide chromatin analysis of a higher eukaryote.
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0.9890 The covalent modification of nucleosomal Proteinhistones has emerged as a major determinant of chromatin structure and gene activity.
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0.9949 To understand the interplay between various Proteinhistone modifications, including acetylation and methylation, we performed a genome - wide chromatin structure analysis in a higher eukaryote.
0.9871 To understand the interplay between various histone modifications, including Acetylationacetylation and methylation, we performed a genome - wide chromatin structure analysis in a higher eukaryote.
0.8893 To understand the interplay between various histone modifications, including acetylation and Methylationmethylation , we performed a genome - wide chromatin structure analysis in a higher eukaryote.
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0.9949 We found a binary pattern of Proteinhistone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.9866 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of ProteinH3 , and inactive genes being hypomethylated and deacetylated at the same residues.
0.9506 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and ProteinH4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.9282 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for ProteinH3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.9132 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.8731 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.8616 We found a binary pattern of histone modifications among euchromatic genes, with active genes being Acetylationhyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.7554 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and Methylationhypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.6054 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being Methylationhypomethylated and deacetylated at the same residues.
0.3837 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and Lys 79 of H3, and inactive genes being hypomethylated and Deacetylationdeacetylated at the same residues.
0.7354 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at Lys 4 and EntityLys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
0.6472 We found a binary pattern of histone modifications among euchromatic genes, with active genes being hyperacetylated for H3 and H4 and hypermethylated at EntityLys 4 and Lys 79 of H3, and inactive genes being hypomethylated and deacetylated at the same residues.
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0.9920 Less frequent promoter DNA_methylationhypermethylation of DLC - 1 gene in primary breast cancers.
0.9892 Less frequent promoter hypermethylation of ProteinDLC - 1 gene in primary breast cancers.
0.9601 Less frequent Entitypromoter hypermethylation of DLC - 1 gene in primary breast cancers.
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0.9988 Absence or low expression of ProteinDLC - 1 , a tumor suppressor gene, in breast cancers has been shown recently.
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0.9993 LOH of 8p12 - p22, on which DLC - 1 is located, is frequent in breast cancers, but the correlation between low expression of ProteinDLC - 1 and LOH has not been confirmed.
0.9977 LOH of 8p12 - p22, on which ProteinDLC - 1 is located, is frequent in breast cancers, but the correlation between low expression of DLC - 1 and LOH has not been confirmed.
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0.9866 To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the DNA_methylationmethylation status of DLC - 1 promoter region in breast cancer cell lines and primary breast tumors.
0.9374 To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of ProteinDLC - 1 promoter region in breast cancer cell lines and primary breast tumors.
0.9167 To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors.
0.9389 To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 Entitypromoter region in breast cancer cell lines and primary breast tumors.
0.8262 To determine the implication of aberrant DNA_methylationmethylation , one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 promoter region in breast cancer cell lines and primary breast tumors.
0.5645 To determine the implication of aberrant methylation, one of the most frequent mechanisms of silencing the tumor suppressor or cancer - related genes, we examined the methylation status of DLC - 1 promoter Entityregion in breast cancer cell lines and primary breast tumors.
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0.9837 The hypermethylation status was examined by MSP and 25 % of cell lines harbored a DNA_methylationmethylated allele.
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0.9996 The gene silencing by methylation was also confirmed by the re - expression of ProteinDLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 hypermethylated cell line.
0.9959 The gene silencing by methylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in ProteinDLC - 1 hypermethylated cell line.
0.9005 The gene silencing by methylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 DNA_methylationhypermethylated cell line.
0.8026 The gene silencing by DNA_methylationmethylation was also confirmed by the re - expression of DLC - 1 by the 5 - aza - 2'- deoxycytidine treatment in DLC - 1 hypermethylated cell line.
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0.9972 But the methylation of ProteinDLC - 1 gene was less frequently shown in primary breast cancers ( 10 % ).
0.9943 But the DNA_methylationmethylation of DLC - 1 gene was less frequently shown in primary breast cancers ( 10 % ).
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0.9911 These data suggest that hypermethylation is responsible for silencing of ProteinDLC - 1 gene in a limited portion of breast cancers.
0.9896 These data suggest that DNA_methylationhypermethylation is responsible for silencing of DLC - 1 gene in a limited portion of breast cancers.
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0.9962 Glycosylation of the ProteinENV spike of primate immunodeficiency viruses and antibody neutralization.
0.9626 GlycosylationGlycosylation of the ENV spike of primate immunodeficiency viruses and antibody neutralization.
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0.9999 The logical target of protective antibody responses elicited by potential HIV vaccines should be the viral ProteinEnv spike on the surface of the virion.
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0.9998 This is thought to be a result of a combination of immunodominance of hypervariable regions of the ProteinEnv protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer.
0.9998 This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the ProteinEnv trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer.
0.9990 This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of ProteinEnv within the trimer.
0.9984 This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to Proteingp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer.
0.9979 This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric Proteingp120 , conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive glycosylation of the exposed regions of Env within the trimer.
0.9382 This is thought to be a result of a combination of immunodominance of hypervariable regions of the Env protein that can easily escape neutralization, antibody reactivity to gp160 " decoy " protein in cell surface debris or monomeric gp120, conformational constraints within the Env trimer that create unfavorable antibody binding conditions and extensive Glycosylationglycosylation of the exposed regions of Env within the trimer.
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0.9996 Part of the strategy toward development of an optimally immunogenic ProteinEnv spike will likely require modification of Env glycosylation.
0.9977 Part of the strategy toward development of an optimally immunogenic Env spike will likely require modification of ProteinEnv glycosylation.
0.9750 Part of the strategy toward development of an optimally immunogenic Env spike will likely require modification of Env Glycosylationglycosylation .
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0.9094 Comparison of methylation - specific polymerase chain reaction ( MSP ) with Proteinreverse transcriptase - polymerase chain reaction ( RT - PCR ) in peripheral blood of gastric cancer patients.
0.7326 Comparison of methylation - specific polymerase chain reaction ( MSP ) with reverse Proteintranscriptase - polymerase chain reaction ( RT - PCR ) in peripheral blood of gastric cancer patients.
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0.9988 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, ProteinE - cadherin , and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients.
0.9987 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for Proteinp16 , E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients.
0.9615 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta Protein( RARbeta ) genes using blood samples from gastric cancer patients.
0.9401 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and Proteinretinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients.
0.9394 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific Proteinreverse transcriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients.
0.8514 This study was designed to compare carcinoembryonic antigen ( CEA ) - specific reverse Proteintranscriptase - polymerase chain reaction ( RT - PCR ) and methylation - specific polymerase chain reaction ( MSP ) for p16, E - cadherin, and retinoic acid receptor beta ( RARbeta ) genes using blood samples from gastric cancer patients.
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0.9973 The MSP assay detected hypermethylation of Proteinp16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ).
0.9958 The MSP assay detected hypermethylation of p16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and ProteinRARbeta in 6 patients ( 15 % ).
0.9950 The MSP assay detected hypermethylation of p16 in 9 patients ( 22 % ), ProteinE - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ).
0.9851 The MSP assay detected DNA_methylationhypermethylation of p16 in 9 patients ( 22 % ), E - cadherin in 9 patients ( 22 % ), and RARbeta in 6 patients ( 15 % ).
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0.4971 Altogether, 18 patients ( 44 % ) showed DNA_methylationhypermethylation .
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0.9985 Superoxide dismutase and Proteincatalase are required to detect (. - ) NO from both coupled and uncoupled neuronal no synthase.
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0.9846 Despite numerous approaches to measuring nitric oxide ( (. - ) NO ) formation from purified NO synthase Protein( NOS ) , it is still not clear whether (. - ) NO is a direct or indirect product of the NO synthase reaction.
0.9135 Despite numerous approaches to measuring nitric oxide ( (. - ) NO ) formation from purified ProteinNO synthase ( NOS ), it is still not clear whether (. - ) NO is a direct or indirect product of the NO synthase reaction.
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0.9993 In conclusion, standard Clark - type ( ) NO electrodes are cross - sensitive to H ( 2 ) O ( 2 ) and therefore both SOD and Proteincatalase are absolutely required to specifically detect (. - ) NO from NOS.
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0.9997 We also found that the transcription of a pathway - specific regulator, Proteingra - ORF9 , was activated by exogenous SAM treatment.
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0.9701 We show that the glucosyltransferase domain of lethal toxin from Clostridium sordellii Protein( LT ( cyt ) ; amino acids 1 - 546 ), which is released into the cytosol during cell infection, binds preferentially to liposomes containing phosphatidylserine as compared with other anionic lipids.
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0.9985 The binding of ProteinLT ( cyt ) to phosphatidylserine increases by two orders of magnitude the rate of glucosylation of liposome - bound geranyl - geranylated Rac - GDP.
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0.9940 Limited proteolysis and deletion studies show that the binding site for phosphatidylserine lies within the first 18 N - terminal residues of ProteinLT ( cyt ) .
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0.9985 Deletion of these residues abolishes the effect of phosphatidylserine on the activity of ProteinLT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by LT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of LT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution.
0.9978 Deletion of these residues abolishes the effect of phosphatidylserine on the activity of LT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by ProteinLT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of LT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution.
0.9972 Deletion of these residues abolishes the effect of phosphatidylserine on the activity of LT ( cyt ) on liposome - bound geranyl - geranylated Rac - GDP and prevents the morphological effects induced by LT ( cyt ) microinjection into various cells, but it does not affect the intrinsic activity of ProteinLT ( cyt ) on non - geranyl - geranylated Rac - GDP in solution.
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0.9984 We conclude that the avidity of ProteinLT ( cyt ) for phosphatidylserine facilitates its targeting to the cytosolic leaflet of cell membranes and, notably, the plasma membrane, where this anionic lipid is abundant and where several targets of lethal toxin reside.
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0.9663 Site - specific substitutions of arginine for lysine in the thermostable D - xylose isomerase Protein( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation.
0.9347 Site - specific substitutions of arginine for lysine in the thermostable ProteinD - xylose isomerase ( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation.
0.5951 Site - specific substitutions of arginine for lysine in the thermostable ProteinD - xylose isomerase ( XI ) from Actinoplanes missouriensis are shown to impart significant heat stability enhancement in the presence of sugar substrates most probably by interfering with nonenzymatic glycation.
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0.9819 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase Protein( GAPDH ) from Bacillus subtilis.
0.9721 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase Protein( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis.
0.9103 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, zinc - superoxide dismutase ( CuZnSOD ) and ProteinD - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis.
0.8498 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human Proteincopper, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis.
0.8003 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper, Proteinzinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis.
0.7742 This rather conservative substitution is moreover shown to improve thermostability in two other structurally unrelated proteins, human copper Protein, zinc - superoxide dismutase ( CuZnSOD ) and D - glyceraldehyde - 3 - phosphate dehydrogenase ( GAPDH ) from Bacillus subtilis.
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0.9960 The stabilizing effect of Lys - - - - Arg substitutions is rationalized on the basis of a detailed analysis of the crystal structures of wild - type ProteinXI and of engineered variants with Lys - - - - Arg substitution at four distinct locations, residues 253, 309, 319, and 323.
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0.9974 Molecular model building analysis of the structures of wild - type and mutant CuZnSOD ( K9R ) and ProteinGAPDH ( G281K and G281R ) is used to explain the observed stability enhancement in these proteins.
0.9869 Molecular model building analysis of the structures of wild - type and mutant ProteinCuZnSOD ( K9R ) and GAPDH ( G281K and G281R ) is used to explain the observed stability enhancement in these proteins.
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0.9929 Human SWI / SNF - associated PRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ST7 and ProteinNM23 tumor suppressor genes.
0.9891 Human SWI / SNF - associated ProteinPRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes.
0.9872 Human SWI / SNF - associated PRMT5 methylates histone H3 arginine 8 and negatively regulates expression of ProteinST7 and NM23 tumor suppressor genes.
0.5813 Human SWI / SNF - associated PRMT5 methylates Proteinhistone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes.
0.5519 Human SWI / SNF - associated PRMT5 methylates histone H3 Entityarginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes.
0.5334 Human SWI / SNF - associated PRMT5 Methylationmethylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes.
Human SWI / SNF - associated PRMT5 Catalysismethylates histone H3 arginine 8 and negatively regulates expression of ST7 and NM23 tumor suppressor genes.
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0.9994 We have recently shown that ProteinPRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4.
0.9992 We have recently shown that PRMT5 can interact with flag - tagged ProteinBRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4.
0.9968 We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and ProteinhBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and H4.
0.9908 We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate histones H3 and ProteinH4 .
0.9304 We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically methylate Proteinhistones H3 and H4.
0.8629 We have recently shown that PRMT5 can interact with flag - tagged BRG1 - and hBRM - based hSWI / SNF chromatin remodelers and that both complexes can specifically Methylationmethylate histones H3 and H4.
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0.9991 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated ProteinPRMT5 .
0.9989 Here we report that ProteinPRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.9927 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and ProteinH4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.9897 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate ProteinH3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.9599 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that ProteinH3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.9479 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and ProteinH4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.9199 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.8236 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 Entityarginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.6727 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of Methylationmethylation by recombinant and hSWI / SNF - associated PRMT5.
0.6351 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 Entityarginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
0.5712 Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can Catalysismethylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of methylation by recombinant and hSWI / SNF - associated PRMT5.
Here we report that PRMT5 can be found in association with endogenous hSWI / SNF complexes, which can methylate H3 and H4 N - terminal tails, and show that H3 arginine 8 and H4 arginine 3 are preferred sites of Catalysismethylation by recombinant and hSWI / SNF - associated PRMT5.
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0.9985 To elucidate the role played by ProteinPRMT5 in gene regulation, we have established a PRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when PRMT5 levels are reduced.
0.9969 To elucidate the role played by PRMT5 in gene regulation, we have established a ProteinPRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when PRMT5 levels are reduced.
0.9962 To elucidate the role played by PRMT5 in gene regulation, we have established a PRMT5 antisense cell line and determined by microarray analysis that more genes are derepressed when ProteinPRMT5 levels are reduced.
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0.9962 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and ProteinhBRM complexes.
0.9935 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing ProteinBRG1 and hBRM complexes.
0.9745 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 Protein( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
0.9604 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of ProteinPRMT5 - containing BRG1 and hBRM complexes.
0.9591 Among the affected genes, we show that suppressor of tumorigenicity 7 Protein( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
0.9141 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and Proteinnonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
0.7518 Among the affected genes, we show that Proteinsuppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
0.9664 Among the affected genes, we show that suppressor of tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of ProteinPRMT5 - containing BRG1 and hBRM complexes.
0.5466 Among the affected genes, we show that suppressor of Proteintumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
0.5392 Among the affected genes, we show that suppressor Proteinof tumorigenicity 7 ( ST7 ) and nonmetastatic 23 ( NM23 ) are direct targets of PRMT5 - containing BRG1 and hBRM complexes.
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0.9998 Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses ProteinPRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
0.9988 Furthermore, we demonstrate that expression of ProteinST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
0.9984 Furthermore, we demonstrate that expression of ST7 and ProteinNM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
0.7305 Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 Methylationmethylation , H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
0.6449 Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, EntityH3K9 deacetylation, and increased transformation of NIH 3T3 cells.
0.5277 Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, H3K9 Deacetylationdeacetylation , and increased transformation of NIH 3T3 cells.
0.5087 Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with EntityH3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with ProteinH3R8 methylation, H3K9 deacetylation, and increased transformation of NIH 3T3 cells.
Furthermore, we demonstrate that expression of ST7 and NM23 is reduced in a cell line that overexpresses PRMT5 and that this decrease in expression correlates with H3R8 methylation, ProteinH3K9 deacetylation, and increased transformation of NIH 3T3 cells.
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0.9970 These findings suggest that the ProteinBRG1 - and hBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression.
0.9871 These findings suggest that the BRG1 - and ProteinhBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression.
0.6126 These findings suggest that the BRG1 - and hBRM - associated ProteinPRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression.
0.8841 These findings suggest that the BRG1 - and ProteinhBRM - associated PRMT5 regulates cell growth and proliferation by controlling expression of genes involved in tumor suppression.
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0.9999 In the current study, we examined the radiation - induced changes in expression of maintenance ProteinDNMT1 , and de novo methyltransferases DNMT3a and DNMT3b in spleen and liver of irradiated animals.
0.9998 In the current study, we examined the radiation - induced changes in expression of maintenance DNMT1, and de novo methyltransferases ProteinDNMT3a and DNMT3b in spleen and liver of irradiated animals.
0.9998 In the current study, we examined the radiation - induced changes in expression of maintenance DNMT1, and de novo methyltransferases DNMT3a and ProteinDNMT3b in spleen and liver of irradiated animals.
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0.9998 We present the data on tissue - specificity in radiation - induced expression of DNA methyltransferases, and prove that changes in the expression of de novo methyltransferases DNMT3a and ProteinDNMT3b are the most important in radiation - induced DNA methylation alterations.
0.9998 We present the data on tissue - specificity in radiation - induced expression of DNA methyltransferases, and prove that changes in the expression of de novo methyltransferases ProteinDNMT3a and DNMT3b are the most important in radiation - induced DNA methylation alterations.
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0.9290 To isolate useful microbial enzymes from uncultured soil microorganisms, a metagenome was isolated from soil samples, and a metagenomic library was constructed by using the ProteinpUC19 vector.
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0.9974 The putative amylase gene Protein( amyM ) was overexpressed and purified for characterization.
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0.9989 Optimal conditions for the enzyme activity of the ProteinAmyM protein were 42 degrees C and pH 9. 0 ; Ca2 + stabilized the activity.
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0.9979 The hydrolysis and transglycosylation properties of ProteinAmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and 4 - alpha - glucanotransferase.
0.9341 The hydrolysis and transglycosylation properties of AmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and Protein4 - alpha - glucanotransferase .
0.4699 The hydrolysis and Glycosylationtransglycosylation properties of AmyM suggest that it has novel characteristics and can be regarded as an intermediate type of maltogenic amylase, alpha - amylase, and 4 - alpha - glucanotransferase.
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0.8859 Protein4 - Hydroxyphenylpyruvate dioxygenase .
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0.9759 4 - Hydroxyphenylpyruvate dioxygenase Protein( HPPD ) is an Fe ( II ) - dependent, non - heme oxygenase that catalyzes the conversion of 4 - hydroxyphenylpyruvate to homogentisate.
0.8469 Protein4 - Hydroxyphenylpyruvate dioxygenase ( HPPD ) is an Fe ( II ) - dependent, non - heme oxygenase that catalyzes the conversion of 4 - hydroxyphenylpyruvate to homogentisate.
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0.9989 ProteinHPPD is a member of the alpha - keto acid dependent oxygenases that typically require an alpha - keto acid ( almost exclusively alpha - ketoglutarate ) and molecular oxygen to either oxygenate or oxidize a third molecule.
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0.9988 As an exception in this class of enzymes ProteinHPPD has only two substrates, does not use alpha - ketoglutarate, and incorporates both atoms of dioxygen into the aromatic product, homogentisate.
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0.9997 The transformation catalyzed by ProteinHPPD has both agricultural and therapeutic significance.
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0.9989 ProteinHPPD catalyzes the second step in the pathway for the catabolism of tyrosine, that is common to essentially all aerobic forms of life.
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0.9989 Naturally occurring multi - ketone molecules act as allelopathic agents by inhibiting ProteinHPPD and preventing the production of homogentisate and hence required redox cofactors.
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0.9983 Interestingly, ProteinHPPD inhibitor / herbicide molecules act also as therapeutic agents for a number of debilitating and lethal inborn defects in tyrosine catabolism by preventing the accumulation of toxic metabolites.
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0.9881 Distinct dynamics and distribution of Proteinhistone methyl - lysine derivatives in mouse development.
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0.9729 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and ProteinH4 .
0.9491 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on Proteinhistones H3 and H4.
0.9373 Histone Methylationmethylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and H4.
0.9284 ProteinHistone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on histones H3 and H4.
0.9095 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of Entityarginine and lysine residues on histones H3 and H4.
0.8980 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4.
0.7104 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and Entitylysine residues on histones H3 and H4.
0.5154 Histone methylation acts as an epigenetic regulator of chromatin activity through the modification of arginine and lysine residues on Proteinhistones H3 and H4.
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0.9925 To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on histone H3 and EntityK20 on histone H4 in midgestation mouse embryos.
0.9920 To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving EntityK9 on histone H3 and K20 on histone H4 in midgestation mouse embryos.
0.9461 To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on Proteinhistone H3 and K20 on histone H4 in midgestation mouse embryos.
0.9343 To examine the potential developmental roles of these modifications, we determined the global patterns of lysine methylation involving K9 on histone H3 and K20 on Proteinhistone H4 in midgestation mouse embryos.
0.9261 To examine the potential developmental roles of these modifications, we determined the global patterns of lysine Methylationmethylation involving K9 on histone H3 and K20 on histone H4 in midgestation mouse embryos.
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0.9743 Interestingly, three of these modifications, histone H3 trimethyl EntityK9 , histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
0.9684 Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl EntityK20 exhibited marked differences in their distribution within the neuroepithelium.
0.9539 Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl EntityK20 , and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
0.9449 Interestingly, three of these modifications, Proteinhistone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
0.9394 Interestingly, three of these modifications, histone H3 trimethyl K9, Proteinhistone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
0.9185 Interestingly, three of these modifications, histone H3 trimethyl K9, histone H4 monomethyl K20, and Proteinhistone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
0.8652 Interestingly, three of these Methylationmodifications , histone H3 trimethyl K9, histone H4 monomethyl K20, and histone H4 trimethyl K20 exhibited marked differences in their distribution within the neuroepithelium.
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0.9887 Specifically, both histone H3 trimethyl K9 and ProteinH4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface.
0.9757 Specifically, both histone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the EntityK9 modification was limited to mitotic cells on the luminal surface.
0.9641 Specifically, both histone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 Methylationmodification was limited to mitotic cells on the luminal surface.
0.9408 Specifically, both Proteinhistone H3 trimethyl K9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface.
0.9344 Specifically, both histone H3 trimethyl EntityK9 and H4 monomethyl K20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface.
0.8709 Specifically, both histone H3 trimethyl K9 and H4 monomethyl EntityK20 were elevated in proliferating cells of the neural tube, which in the case of the K9 modification was limited to mitotic cells on the luminal surface.
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0.9584 In contrast, Proteinhistone H4 trimethyl K20 was progressively lost from these medial regions and became enriched in differentiating neurons in the ventrolateral neural tube.
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0.9813 The inverse relationship of histone H4 EntityK20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
0.9358 The inverse relationship of Proteinhistone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
0.9302 The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
0.9676 The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the Methylationtrimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
0.7513 The inverse relationship of histone H4 K20 Methylationmethyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl modification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
0.7046 The inverse relationship of histone H4 K20 methyl derivatives is even more striking during skeletal and cardiac myogenesis where the accumulation of the trimethyl Methylationmodification in pericentromeric heterochromatin suggests a role in gene silencing in postmitotic muscle cells.
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0.9796 Importantly, our results establish that histone lysine Methylationmethylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation.
0.9606 Importantly, our results establish that histone Entitylysine methylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation.
0.9308 Importantly, our results establish that Proteinhistone lysine methylation occurs in a highly dynamic manner that is consistent with their function in an epigenetic program for cell division and differentiation.
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0.9997 Decreased expression of lysyl hydroxylase 2 ( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the ProteinLH2 gene.
0.9692 Decreased expression of lysyl hydroxylase 2 Protein( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the LH2 gene.
0.8437 Decreased expression of Proteinlysyl hydroxylase 2 ( LH2 ) in skin fibroblasts from three Ehlers - Danlos patients does not result from mutations in either the coding or proximal promoter region of the LH2 gene.
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0.9967 These patients have significantly decreased levels of lysyl hydroxylase ( LH ) activity, due to mutations in the ProteinLH1 gene.
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0.6730 LH Hydroxylationhydroxylates specific lysine residues in the collagen molecule that are precursors for the formation of cross - links which provide collagen with its tensile strength.
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0.9988 No disorder has been directly linked to decreased expression of LH2 and ProteinLH3 , two other isoforms of LH.
0.9988 No disorder has been directly linked to decreased expression of ProteinLH2 and LH3, two other isoforms of LH.
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0.9987 This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for LH2, but normal levels of LH1 and ProteinLH3 mRNAs, in their skin fibroblasts.
0.9984 This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for ProteinLH2 , but normal levels of LH1 and LH3 mRNAs, in their skin fibroblasts.
0.9979 This study describes 3 patients with mixed phenotypes of EDS, who have significantly decreased mRNAs for LH2, but normal levels of ProteinLH1 and LH3 mRNAs, in their skin fibroblasts.
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0.9985 In contrast to the effect of ProteinLH1 deficiency in EDS VI patients, the decreased expression of LH2 does not affect LH activity, bifunctional collagen cross - links ( measured after reduction as dihydroxylysinonorleucine ( DHLNL ) and hydroxylysinonorleucine ( HLNL ) ), or helical lysine hydroxylation in these cell lines.
0.9984 In contrast to the effect of LH1 deficiency in EDS VI patients, the decreased expression of ProteinLH2 does not affect LH activity, bifunctional collagen cross - links ( measured after reduction as dihydroxylysinonorleucine ( DHLNL ) and hydroxylysinonorleucine ( HLNL ) ), or helical lysine hydroxylation in these cell lines.
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0.9995 Sequence analysis of full length LH2 cDNAs and 1kb of the promoter region of ProteinLH2 does not show mutations that could explain the decreased expression of LH2.
0.9995 Sequence analysis of full length LH2 cDNAs and 1kb of the promoter region of LH2 does not show mutations that could explain the decreased expression of ProteinLH2 .
0.9986 Sequence analysis of full length ProteinLH2 cDNAs and 1kb of the promoter region of LH2 does not show mutations that could explain the decreased expression of LH2.
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0.9996 These results suggest that the deficiency of ProteinLH2 in these fibroblasts may be caused by changes in other factors required for the expression of LH2.
0.9995 These results suggest that the deficiency of LH2 in these fibroblasts may be caused by changes in other factors required for the expression of ProteinLH2 .
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0.9998 Expression and purification of functionally active hyaluronan - binding domains from human cartilage link protein, aggrecan and Proteinversican : formation of ternary complexes with defined hyaluronan oligosaccharides.
0.9995 Expression and purification of functionally active hyaluronan - binding domains from human cartilage link protein, Proteinaggrecan and versican : formation of ternary complexes with defined hyaluronan oligosaccharides.
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0.9984 The chondroitin sulfate proteoglycan Proteinaggrecan forms link protein - stabilized complexes with hyaluronan ( HA ), via its N - terminal G1 - domain, that provide cartilage with its load bearing properties.
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0.9993 Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, brevican, and neurocan ) substitute for Proteinaggrecan , may contribute to the structural integrity of many other tissues including skin and brain.
0.9986 Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, Proteinbrevican , and neurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain.
0.9986 Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. Proteinversican , brevican, and neurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain.
0.9984 Similar aggregates ( potentially containing new members of the link protein family ), in which other chondroitin sulfate proteoglycans ( i. e. versican, brevican, and Proteinneurocan ) substitute for aggrecan, may contribute to the structural integrity of many other tissues including skin and brain.
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0.9983 In this study, cartilage link protein ( cLP ) and the G1 - domains of Proteinaggrecan ( AG1 ) and versican ( VG1 ) were expressed in Drosophila S2 cells.
0.9975 In this study, cartilage link protein ( cLP ) and the G1 - domains of aggrecan ( AG1 ) and Proteinversican ( VG1 ) were expressed in Drosophila S2 cells.
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0.9383 The recombinant human proteins were found to have properties similar to those described for the native molecules ( e. g. cLP was able to form oligomers, and ProteinHA decasaccharides were the minimum size that could compete effectively for their binding to polymeric HA ).
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0.9996 Surprisingly, the length of HA required to accommodate two G1 - domains was found to be significantly larger for aggrecan than Proteinversican , which may reflect differences in the conformation of HA stabilized on binding these proteins.
0.9995 Surprisingly, the length of HA required to accommodate two G1 - domains was found to be significantly larger for Proteinaggrecan than versican, which may reflect differences in the conformation of HA stabilized on binding these proteins.
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0.9968 Protective mechanism of epigallocatechin - 3 - gallate against Helicobacter pylori - induced gastric epithelial cytotoxicity via the blockage of ProteinTLR - 4 signaling.
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0.9995 To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated ProteinTLR - 4 were carried out.
0.9909 To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to Glycosylationglycosylated TLR - 4 were carried out.
0.9659 To investigate the effect of EGCG on H. pylori - induced toll - like receptor 4 Protein( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated TLR - 4 were carried out.
0.7672 To investigate the effect of EGCG on H. pylori - induced Proteintoll - like receptor 4 ( TLR - 4 ) signaling, reverse transcription - polymerase chain reaction and Western blot analysis corresponding to glycosylated TLR - 4 were carried out.
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0.9991 Helicobacter pylori infection stimulated the glycosylation of ProteinTLR - 4 , which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 glycosylation.
0.9966 Helicobacter pylori infection stimulated the glycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the ProteinTLR - 4 glycosylation.
0.9873 Helicobacter pylori infection stimulated the Glycosylationglycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 glycosylation.
0.9561 Helicobacter pylori infection stimulated the glycosylation of TLR - 4, which initiates intracellular signaling in the infected host cell, but the pretreatment with EGCG completely blocked the TLR - 4 Glycosylationglycosylation .
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0.9998 The blockage of ProteinTLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori.
0.9996 The blockage of TLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of ProteinTLR - 4 signaling induced by H. pylori.
0.9632 The blockage of TLR - 4 activation by EGCG resulted in inactivation of extracellular signal response kinase Protein1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori.
0.7716 The blockage of TLR - 4 activation by EGCG resulted in inactivation of Proteinextracellular signal response kinase 1 / 2 and of nuclear factor - kappaB, the downstream molecules of TLR - 4 signaling induced by H. pylori.
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0.9979 CONCLUSIONS : EGCG pretreatment showed significant cytoprotective effects against H. pylori - induced gastric cytotoxicity via interference of the ProteinTLR - 4 signaling induced by H. pylori.
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0.9966 Bare - faced curassow Proteinlysozyme carrying amino acid substitutions at subsites E and F shows a change in activity against chitooligosaccharide caused by a local conformational change.
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0.9737 A new form of avian lysozyme, bare - faced curassow Proteinlysozyme ( BCL ), was purified and chemically sequenced.
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0.9986 Of the 26 substitutions relative to chicken Proteinlysozyme , three, F34Y, T47S, and R114H, are of substrate - interacting residues in the E and F subsites, which would contribute to the acceptor binding for transglycosylation.
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0.9817 T47S is a novel substitution in this Proteinlysozyme class.
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0.9987 While other Proteinlysozymes also have substitutions at positions 114 and 34, they also contain numerous others, including ones in the other substrate binding sites, A - D.
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0.9946 MD simulation analysis of BCL suggested that the substituted amino acids changed the local conformation of this Proteinlysozyme at the E - F sites.
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0.9727 Histone H2B Ubiquitinationubiquitylation is associated with elongating RNA polymerase II.
0.9419 ProteinHistone H2B ubiquitylation is associated with elongating RNA polymerase II.
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0.9673 Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine Methylationmethylation on histone H3.
0.9612 Rad6 - mediated Ubiquitinationubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3.
0.9571 Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on Proteinhistone H3 .
0.9294 Rad6 - mediated ubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3.
0.9205 Rad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of Entitylysine methylation on histone H3.
0.9110 ProteinRad6 - mediated ubiquitylation of histone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3.
0.8977 Rad6 - mediated ubiquitylation of Proteinhistone H2B at lysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3.
0.5465 Rad6 - mediated ubiquitylation of histone H2B at Entitylysine 123 has been linked to transcriptional activation and the regulation of lysine methylation on histone H3.
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0.9952 However, how ProteinRad6 and H2B ubiquitylation contribute to the transcription and histone methylation processes is poorly understood.
0.9940 However, how Rad6 and ProteinH2B ubiquitylation contribute to the transcription and histone methylation processes is poorly understood.
0.9820 However, how Rad6 and H2B ubiquitylation contribute to the transcription and Proteinhistone methylation processes is poorly understood.
0.9460 However, how Rad6 and H2B Ubiquitinationubiquitylation contribute to the transcription and histone methylation processes is poorly understood.
0.8440 However, how Rad6 and H2B ubiquitylation contribute to the transcription and histone Methylationmethylation processes is poorly understood.
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0.9996 Here, we show that the ProteinPaf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ).
0.9991 Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, ProteinBre1 , mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ).
0.9991 Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of ProteinRad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ).
0.9979 Here, we show that the Paf1 transcription elongation complex and the E3 ligase for ProteinRad6 , Bre1, mediate an association of Rad6 with the hyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ).
0.6980 Here, we show that the Paf1 transcription elongation complex and the E3 ligase for Rad6, Bre1, mediate an association of Rad6 with the Phosphorylationhyperphosphorylated ( elongating ) form of RNA polymerase II ( Pol II ).
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0.9982 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or ProteinBre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.9962 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various ProteinPaf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.9946 This association appears to be necessary for the transcriptional activities of ProteinRad6 , as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.9924 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation ( ubH2B ) and reduces the recruitment of ProteinRad6 to the promoters and transcribed regions of active genes.
0.9870 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes ProteinH2B ubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.9690 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.9536 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B ubiquitylation Protein( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
0.5365 This association appears to be necessary for the transcriptional activities of Rad6, as deletion of various Paf1 complex members or Bre1 abolishes H2B Ubiquitinationubiquitylation ( ubH2B ) and reduces the recruitment of Rad6 to the promoters and transcribed regions of active genes.
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0.9999 Using the inducible ProteinGAL1 gene as a model, we find that the recruitment of Rad6 upon activation occurs rapidly and transiently across the gene and coincides precisely with the appearance of Pol II.
0.9989 Using the inducible GAL1 gene as a model, we find that the recruitment of ProteinRad6 upon activation occurs rapidly and transiently across the gene and coincides precisely with the appearance of Pol II.
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0.9997 Significantly, during ProteinGAL1 activation in an rtf1 deletion mutant, Rad6 accumulates at the promoter but is absent from the transcribed region.
0.9996 Significantly, during GAL1 activation in an Proteinrtf1 deletion mutant, Rad6 accumulates at the promoter but is absent from the transcribed region.
0.9977 Significantly, during GAL1 activation in an rtf1 deletion mutant, ProteinRad6 accumulates at the promoter but is absent from the transcribed region.
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0.9993 This fact suggests that Rad6 is recruited to promoters independently of the ProteinPaf1 complex but then requires this complex for entrance into the coding region of genes in a Pol II - associated manner.
0.9989 This fact suggests that ProteinRad6 is recruited to promoters independently of the Paf1 complex but then requires this complex for entrance into the coding region of genes in a Pol II - associated manner.
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0.9991 In support of a role for Rad6 - dependent H2B ubiquitylation in transcription elongation, we find that ProteinubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation.
0.9976 In support of a role for Rad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of ProteinKin28 , the serine 5 CTD kinase that promotes the transition from initiation to elongation.
0.9699 In support of a role for Rad6 - dependent H2B Ubiquitinationubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation.
0.9572 In support of a role for Rad6 - dependent ProteinH2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation.
0.9026 In support of a role for ProteinRad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation.
0.8137 In support of a role for ProteinRad6 - dependent H2B ubiquitylation in transcription elongation, we find that ubH2B levels are dramatically reduced in strains bearing mutations of the Pol II C - terminal domain ( CTD ) and abolished by inactivation of Kin28, the serine 5 CTD kinase that promotes the transition from initiation to elongation.
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0.9979 Furthermore, synthetic genetic array analysis reveals that the ProteinRad6 complex interacts genetically with a number of known or suspected transcription elongation factors.
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0.9909 Finally, we show that Saccharomyces cerevisiae mutants bearing defects in the pathway to ProteinH2B ubiquitylation display transcription elongation defects as assayed by 6 - azauracil sensitivity.
0.9725 Finally, we show that Saccharomyces cerevisiae mutants bearing defects in the pathway to H2B Ubiquitinationubiquitylation display transcription elongation defects as assayed by 6 - azauracil sensitivity.
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0.9955 Collectively, our results indicate a role for Rad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which ProteinH3 methylation may be regulated.
0.9910 Collectively, our results indicate a role for Rad6 and ProteinH2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated.
0.9833 Collectively, our results indicate a role for ProteinRad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated.
0.9372 Collectively, our results indicate a role for Rad6 and H2B Ubiquitinationubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 methylation may be regulated.
0.8328 Collectively, our results indicate a role for Rad6 and H2B ubiquitylation during the elongation cycle of transcription and suggest a mechanism by which H3 Methylationmethylation may be regulated.
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0.9972 Glycosylation - related gene expression in prion diseases : ProteinPrPSc accumulation in scrapie infected GT1 cells depends on beta - 1, 4 - linked GalNAc - 4 - SO4 hyposulfation.
0.9940 Glycosylation - related gene expression in Proteinprion diseases : PrPSc accumulation in scrapie infected GT1 cells depends on beta - 1, 4 - linked GalNAc - 4 - SO4 hyposulfation.